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A HANDBOOK 



PATHOLOGICAL ANATOMY 



AKD 



HISTOLOGY 



WITH AN INTRODUCTORY SECTION ON 

POST-MORTEM EXAMINATIONS 

AND 

THE METHODS OF PRESERVING AND EXAMINING 
DISEASED TISSUES 



BY 

FRANCIS DEL AFIELD, M.D., 

PROFESSOR OF PATHOLOGY AND PRACTICAL MEDICINE, COLLEGE OF PHYSICIANS AND SURGEONS, 

NEW YORK, 



T. MITCHELL PRUDDENT, M.D. 



J 

DIRECTOR OF THE LABORATORY OF THE ALUMNI ASSOCIATION OF THE COLLEGE OF PHYSICIANS AND 

SURGEONS, NEW YORK 



'RIGHT ^ 

( OCT 171889 

THIRD EDITION 

224 WOOD ENGRAVING 



NEW YORK 
WILLIAM WOOD & COMPANY 

1889 



Copyright by 
WILLIAM WOOD & COMPANY. 

1889. 



PRESS OF 

8TETTIHER, LAMBERT A C( 

22, 24 * 2« READE ST., 

NEW YORK. 



PREFACE 

TO THE THIRD EDITION. 



In the third edition of this work, the same objects have been kept in 
view as in the second edition. 

It is intended that the student and the practitioner shall find in it 
the information which they need to enable them to perform autopsies, 
to preserve the tissues, to prepare them properly, and to examine them 
with the microscope. 

The work, therefore, comprises instruction in the methods of making 
post-mortem examinations, of preserving diseased tissues, of preparing 
them for microscopical examination, and of cultivating and examining 
bacteria. It also gives an account of the lesions of the different parts 
of the body, of the general diseases, of violent deaths, and of poisoning; 
of the changes produced by inflammation and degeneration; and of the 
structure of tumors. 

All of the drawings have been made by the authors. 

FRANCIS DELAFIELD, 
T. MITCHELL PRUDDEN. 



CONTENTS. 



PART FIKST. 

THE METHOD OF MAKING POST-MORTEM EXAMINATIONS AND OF 
PRESERVING DISEASED TISSUES. 

The objects of making post-mortem examinations. Causes of death, 3. — External 
Inspection, 4. — Cadaveric lividity, 4. — Putrefactive changes, 5. — Cooling of the 
body, 5. — Rigor mortis, 6. — Contusions, 7. — Wounds, fractures, scars, and tattoo 
marks, 8. — Internal Examination, 8. — The Head, 9.— Removal of calvarium, 
9. — The dura mater, 10. — The pia mater, 10. — The brain, 10. — Methods of open- 
ing the brain, 11-14. — Base of the cranium, 14. — Hardening and preserving the 
tissues for microscopical examination, 15. — The Spinal Cord, 16. — Preservation 
of cord and membranes, 17. — The Thorax and Abdomen, 17. — General inspection 
of abdominal cavity, 18. — The heart, 20. — The pleural cavities, 23. — The lungs, 
23. — Preservation of lungs and bronchi, 24. — Pharynx, larynx, and oesophagus, 
24. — Preservation of larynx and trachea, 25. — The Abdomen, 25. — Kidneys, 25. — 
Suprarenal capsules, 27. — Preservation of kidney, 27. — The spleen, 27. — Preserva- 
tion of suprarenal capsules and spleen, 27-28. — Intestines, 28.— Preservation of 
intestines and stomach, 29 and 30. — Stomach and duodenum, 29. — Liver, 30. — 
Preservation of liver, 31. — Pancreas, 31. — Genito-urinary Organs. Male organs, 
32.— Female organs, 32.— Bladder, 33.— Uterus, 33.— Ovaries and Fallopian tubes, 
34. — Preservation of generative organs, 34. 

Autopsies in Cases op Suspected Poisonlng, 35. 

Examination of the Bodies of New-born Children. General Inspection, 35. — 
Internal Examination, 39. — Preservation of fcetal and young tissues, 42. 

General Methods of Preserving Tissues and Preparing them for Study, 43. 
— Fresh tissues, 43. — Decalcifying, 43. — Hardening and preservation, 44. — Dela- 
field's osmic acid mixture, 44. — Chromic acid mixture, osmic acid, 45. — Imbed- 
ding and section cutting, 46-47. — Staining, 47. — Preservation of museum speci- 
mens, 48. 

PAET SECOND. 

CHANGES IN THE CIRCULATION OF THE BLOOD.— CHANGES IN 
THE COMPOSITION OF THE BLOOD.— DEGENERATIONS.— ANIMAL 
PARASITES AND BACTERIA.— INFLAMMATIONS.— TUMORS. 

Changes in the Circulation of the Blood. Hyperemia and Anaemia, 53.— 
Haemorrhage and transudation, 53. — Thrombosis and embolism, 55. — Infarc- 
tions, 57. 

Changes in the Composition of the Blood. Coagulability of the blood, an- 



VI CONTENTS. 

hydremia and hydremia, 59. — Leucocytosis, leukaemia, melanaemia, 60. — Foreign 
bodies in blood, 61. 

Degenerative Changes in the Tissues. Necrosis and coagulation necrosis, 63. 
— Cheesy degeneration, 64. — Parenchymatous degeneration, 64. — Fatty degenera- 
tion and fatty infiltration, 65. — Amyloid degeneration, 66. — Corpora amylacea, 
67.— Mucoid and colloid degeneration, 67. — Hyaline and calcareous degeneration, 
68. — Pigmentation, 69. 

Animal Parasites. Protozoa. Amoeba, psorospermiae, 70. — Cercomonas intes- 
tinalis, Trichomonas vaginalis, 71.— Ciliated infusoria, 71. — Worms, 71. — Trema- 
toda (flukes), Distoma hepaticum; D. lanceolatum, D. sinense, D. haematobium, 
71-72. — Cestoda (tape worms), 72. — Taenia solium and T. mediocanellata, 72. — T. 
echinococcus, 73. — Echinococcus multilocularis, Taenia nana, 75. — T. flavo- 
punctata, T. madagascariensis, T. cucumerina, 76. — Bothriocephalus latus, 76. — 
Nematoda (round worms), Ascaris lumbricoides, 76. — A. maritima, A. mys- 
tax, Oxyuris vermicularis, Strongylus gigas, Dochmius duodenalis, 77. — 
Tricocephalus dispar, Trichina spiralis, 78. — Filaria medinensis, Filaria sanguinis 
hominis, 80. — Rhabdonema strongyloides, 81. 

Arthropods. Sarcoptes hominis, Pediculus capitis, 81. — Methods of study and 
preparation of internal parasites, bibliography of animal parasites, 82. 

Vegetable Parasites. Parasitic Fungi. Moulds and yeasts, Achorion Schon- 
leinii, Trichophyton tonsurans, Microsporon furfur, Aspergillus, Oidium albicans, 
Actinomycosis, 83. t 

Bacteria. Morphology and physiology, 84: — Classification of bacteria, 86. — Sphe- 
roidal bacteria, micrococcus, diplococcus, streptococci, 87. — Bod-shaped or filiform 
bacteria, bacilli, 88. — Bacilli of septicaemia of mice and of malignant oedema, 89. 
— Leptothrix, 90. — Spiral-shaped bacteria, spirillum, spirochaete, 90. — Saprophy- 
tic and parasitic bacteria, 91. — The relations of bacteria to disease, 91. — Conditions 
influencing the occurrence of bacterial diseases, 94. — Phagocytes, 95. — Methods of 
studying the bacteria, 96. — To stain bacteria, 96, 97, 98. — The microscope, 98. — 
Artificial cultivation of bacteria, 99. — The preparation and use of culture sub- 
stances: potatoes, nutrient gelatin, nutrient agar, beef-tea, milk, 100, 101. — Plate 
cultures, 102. — Bibliography, 103. 

Inflammation. Exudative inflammation, 104.— Croupous inflammation, 107. — Pro- 
ductive inflammation, 110. — Tubercular inflammation, 111. — Syphilitic inflamma- 
tion, acute degeneration, 113. 

Tumors, 115.— General characters, 115, 116, 117, 118.— Cause of tumors, 119.— Classi- 
fication of tumors, 120. — Cysts, 122. — Nomenclature of complex tumors, 124. — 
Special forms of tumors, Fibroma, 125.— Myxoma, 126, 127.— Sarcoma, 128-136.— 
Endothelioma, 136.— Lipoma, Chondroma, 137.— Osteoma, Glioma, 139.— Myoma, 
141.— Neuroma, 142, 143.— Angioma, 144.— Lymphangioma, 145.— Epithelial 
tumors, 146.— Adenoma, 148. — Carcinoma, 150-160.— Bibliography of tumors, 
160. 

PART THIRD. 

MORBID ANATOMY OF THE ORGANS. 

The Nervous System, The Membranes of the Brain, 163.— Dura mater, 
haemorrhages, thrombosis of venous sinuses, 163. — Inflammation, 164, 165, 166. 
—Tumors, 167.— Pia mater, 167. — Hyperaemia, oedema, and haemorrhage, 169.— 
Inflammation, acute meningitis, cellular meningitis, 170. — Exudative meningitis, 
171.— Chronic meningitis, 173.— Tubercular meningitis, 173.— Syphilitic meningi- 
tis, tumors and parasites, 177.— Ventricles of the brain, ependyma and choroid 



CONTENTS. Vll 

plexus, 177. — Acute ependymitis, chronic ependymitis, 178. — Congenital hydro- 
cephalus, 179. — Secondary hydrocephalus, primary hydrocephalus in adults, 
tumors, 180. — Pineal gland, pituitary body, 181. 

The Brain, 181. — Thrombosis and embolism, 181, 182, 183.— Hyperemia, anaemia } 
oedema, and haemorrhage, 184. — Apoplectic foci, 185. — Secondary degenerations, 
187. — Inflammation of the brain, abscesses, 187.— Chronic interstitial encephalitis 
(sclerosis), 189. — Wounds, 189. — Encephalitis in new-born, holes or cysts in brain, 
190. — Syphilitic and tubercular encephalitis, 191. — Lesions of brain in chronic 
paralysis of insane, 192. — Hypertrophy, atrophy, and pigmentation, 193, 194. — 
Tumors, 194.— Parasites, malformations, 195, 196. 

Spinal Cord, 197. — Dura mater spinalis; haemorrhages, inflammation, and tumors, 
197. — Parasites, 198. — Pia mater spinalis; haemorrhages, inflammations, and 
tumors, 198. — The cord; haemorrhage, injuries, and secondary degenerations, 199. 
— Descending gray degeneration, 200. — Ascending gray degeneration, 201. — In- 
flammation, acute myelitis, 202. — Poliomyelitis anterior, 203. — Chronic myelitis, 
chronic interstitial myelitis, chronic transverse myelitis, multiple sclerosis, 205. — 
Posterior spinal sclerosis, 206. — Solitary tubercles, gummata, cysts, and tumors, 
207.— Syringomyelia, 208.— Malformations, 209. 

The Peripheral Nerves. Changes after division, acute neuritis, 210. — Chronic 
neuritis, multiple neuritis, syphilitic and tubercular neuritis, 211. — Leprous neu- 
ritis, tumors, 212. 

Preparation of nerve tissue for microscopical study, 212. 

The Respiratory System. Larynx and Trachea, 214. — Malformations, 214. — Acute 
catarrhal laryngitis and tracheitis, 214. — Chronic catarrhal, croupous, and syphili- 
tic laryngitis, 215. — Tubercular laryngitis, 216. — (Edema glottidis, 217. — Tumors, 
217. 

The Pleura. Hydrothorax, haemorrhage, classification of inflammation, 218. — Pleu- 
risy with production of fibrin, pleurisy with production of fibrin and serum, 219. 
Pleurisy with production of fibrin, serum, and pus (Empyaema), 223. — Chronic 
pleurisy, tubercular pleurisy, 224. — Tumors, 226. 

The Bronchi. Acute catarrhal bronchitis, 227. — Chronic catarrhal bronchitis, acute 
croupous bronchitis, chronic croupous bronchitis, 228. — Bronchiectasia, 229. — 
Tumors, 230. 

The Lungs. Malformations, 231. — Injuries, congestion and oedema, haemorrhage, 
232. — Emphysema, 233. — Atelectasis, gangrene, 235. — Inflammation, classifica- 
tion, acute lobar pneumonia, 236. — Broncho-pneumonia, 241. — Secondary and 
complicating pneumonia, 245. — Pneumonia of heart disease, 247. — Interstitial 
pneumonia, 248. — Tubercular pneumonia, 249. — Acute miliary tuberculosis, 250. 
— Chronic miliary tuberculosis, 254. — Acute pulmonary phthisis, 256. — Chronic 
phthisis, 257. — Syphilitic pneumonia, 260. — Tumors, 262. — Parasites, 263. 

The Mediastinum. Inflammation, 263. — Tumors, 264. 

The Vascular System. Pericardium. Injuries, dropsy, haemorrhage, pneumona- 
tosis, 266.— Inflammation, 267, 268.— Tumors, 268. 

The Heart. Malformations, 268. — Abnormal size and positions of heart, 270. — 
Wounds and ruptures, 271. — Atrophy and hypertrophy, 272. — Dilatation and 
degenerations, 274.— Fatty infiltrations, atrophy of pericardial fat, myomalacia, 
276. — Inflammation, 277. — Simple acute endocarditis, 278. — Mycotic endocar- 
ditis, 279. — Chronic, chronic ulcerative, and tubercular endocarditis, 280. — Myo- 
carditis, 281, 282. — Changes in heart valves, aneurism of the heart, 282. — Throm- 
bosis of the heart, 283. — Tumors and parasites, 284. 

The Blood Vessels. Atrophy and hypertrophy, degeneration, 284. The Arteries, 



Vlll CONTENTS. 

acute and chronic arteritis, 285.— Dilatation and aneurism, 290. — Aneurisms 
of the different arteries, 291.— Stenosis, 292.— Ruptures and wounds, 293. 

The Veins. Dilatation, 295. — Wounds, rupture, and inflammation, 296, 297. — 
Tumors and parasites, 298. — The Capillaries, 298. 

The Lymph Vessels. Inflammation, 299. — Lymphangiectasis, tumors, 300. 

The Lymph Nodes (Lymph Glands), 300. — Acute inflammation, 301. — Chronic 
inflammation, 303. — Pigmentation, 304.— Inflammation with cheesy degeneration, 
305. — Tubercular inflammation, 306. — Syphilitic inflammation and degeneration, 
307. -Hyperplasia, 308.— Tumors and parasites, 309. 

The Alimentary Canal. The Mouth, (malformations, 310. — Hypertrophy, inflam- 
mation, Stomatitis ulcerosa, 311. — Gangrene, tumors, 312. — The Tongue, mal- 
formations, hypertrophy, inflammation, 313. — Tumors, 314. — The Pharynx and 
Oesophagus, inflammation, 315. — Ulceration, dilatation, 316. — Stenosis, tumors, 
317. 

The Stomach. Malformations, 319. — Post-mortem changes, injuries, haemorrhage, 
320. — Inflammation, 321. — Croupous and suppurative gastritis, 322. — Toxic gas- 
tritis, ulcers of the stomach, 323. — Dilatation, tumors, 326. — Degenerations, 329. 

The Intestines. Malformations, 329. — Incarceration, 330. — Intussusception, 331. — 
Transposition, wounds and ruptures, 332. — The Small Intestine, inflammation, 
332. — Lesions of the solitary and agminated glands, 333. — Ulcers of the duode- 
num, syphilitic ulcers, emboli, 334. — The Large Intestine, inflammations, 334. 
— The solitary follicles, caecum, rectum, and vermiform appendix, 336. — Tu- 
mors, 337. — Concretions, parasites, 338. 

The Peritoneum. Malformations, inflammation, 339. — Acute peritonitis, 340. — 
Chronic peritonitis, 343. — Tumors, 347. — Parasites, 349.. 

The Liver. Malformations, acquired changes in position, 350. — Anaemia and 
hyperaemia, 351. — Wounds, rupture, and haemorrhage, lesions of the hepatic 
artery and portal vein, 353. — The hepatic veins, atrophy of the liver, degenera- 
tive changes, 355. — Fatty infiltration, 356. — Fatty degeneration, amyloid degen- 
eration, 357. — Pigmentation, 358. — Acute yellow atrophy, 359. — Inflammation, 
360. — Chronic interstitial hepatitis, 362. — Syphilitic hepatitis, 365. — Tubercular 
hepatitis, 366. — Perihepatitis, hyperplasia of lymphatic tissue, 368. — Tumors, 
369.— Parasites, 371. 

The Biliary Passages. Inflammation, 373. — Constriction and occlusion, 374. — Dilata- 
tion, biliary calculi, 375. — Tumors, 377. 

The Spleen. Wounds, rupture, and haemorrhage, 378. — Disturbances of the circu- 
lation, 379.— Infarctions, 380. — Inflammation, 381. — Perisplenitis, 385. — Altera- 
tions in leukaemia and pseudo-leukaemia, 385.— Degenerative changes, 386. — 
Tumors, parasites, malformations and displacements, 387. 

The Pancreas. Haemorrhage, inflammation, 389. — Degenerative changes, 390. — 
Tumors, 391. — Malformations and displacements, 392. 

The Salivary Glands. Inflammation, 394. — Tumors, parasites, 395. 

The Thyroid Gland. Hyperaemia, inflammation, degenerations, tumors, 396. — 
Parasites, 397. — Myxoedema, 397. 

The Thymus. Haemorrhages, inflammation, 399. 

The Suprarenal Capsules. Malformations, haemorrhage, thrombosis, inflamma- 
tion, degeneration, 400. — Tumors, 401. 

The Urinary xIpparatus. The Kidney, malformations, changes in position, 402. 
— Bright's disease, 403-413. — Suppurative nephritis and pyelo-nephritis, 413. — 
Tubercular nephritis, embolism, and thrombosis, 415. — Hydronephrosis, cystic 
kidney, 416. — Perinephritis, 417. — Renal calculi, tumors, 418. — Parasites, 420. 

The Urinary Bladder. Malformations, 420. — Changes in size and position, 421. — 



CONTENTS. IX 

Rupture, perforation, disturbances in circulation, 422. — Inflammation, 423. — 
Tumors, 424. — Parasites and calculi, 425. 

The Urethra. Malformations, changes in size and position, 427. — Injuries, inflamma- 
tion, 428.— Tumors, 430. 

Organs of Generation. Female. The Vulva, malformations, haemorrhage, 431. 
— Inflammation, tumors, 432. 

The Vagina. Malformations, 433. — Changes in size and position, 434. — Wounds, per- 
foration, inflammation, 435. — Tumors, parasites, 436. — The Uterus, malforma- 
tions, 436. — Changes in size, 437. — Changes in position, 438. — Rupture, perfora- 
tion, hyperemia, haemorrhage, 440. — Inflammation of the unimpregnated uterus, 
442. — Inflammation of the pregnant uterus, 445. — Ulceration and degeneration, 
446. — Tumors, 447. — Parasites and cysts, 452. 

The Ovaries. Malformations, changes in size and position, hyperaemia and haemor- 
rhage, 453. — Inflammation, 454. — Tumors, 456. 

The Fallopian Tubes. Malformations, 460. — Changes in position and size, haemor- 
rhages, inflammation, 461. — Tumors, extra-uterine pregnancy, 462. 

The Placenta. Haemorrhage, 463. — Inflammation, degenerations, 464. 

Tlie Mamma. Malformations, 464. — Haemorrhage, inflammation, 465. — Tumors, 467. 

Organs of Generation. Male. The Penis, malformations, 470. — Inflammation, 
tumors, 472. — The Scrotum, 473. — The Testicles, malformations, hydrocele, 474. 
— Spermatocele, haematocele, 475. — Inflammation, 476. — Tumors, 479. — Parasites, 
480.— The Seminal Vesicles, 480.— The Prostate, hypertrophy, 480.— Inflamma- 
tion, tumors, parasites, concretions, 481. — The Male Mamma, 482. 

The Bones. Disturbances of circulation, injuries, 483. — Inflammation, 484. — Peri- 
ostitis, 484, 485.— Osteitis, 486.— Osteomyelitis, 492.— Necrosis, 493.— Caries, 494. 
— Rachitis, 495.— Osteomalacia, 497. — Alterations of the bone marrow in leukae- 
mia and anaemia, 498. — Atrophy, 499. — Tumors, 500. — Parasites, 503. 

Diseases of the Joints. Inflammation, 504.— Tumors, 507. 

Muscle. Haemorrhage, infarction, wounds and ruptures, inflammation, 509. — Atrophy, 
512. — Pseudo-hypertrophy, 514. —Degenerations, 515. — Hypertrophy, tumors, 
516.— Parasites, 517. 

PART FOUBTH. 

THE LESIONS FOUND IN THE GENERAL DISEASES, IN POISONING, 
AND IN VIOLENT DEATHS. 

Typhoid Fever. Primary or Characteristic Lesions, 521. — The Intestines, 521. — 
Lesions of the lymphatic apparatus, 522.— Gangrene, 523. — Croupous inflamma- 
tion, peritonitis, infarctions, haemorrhage, 524. — Lesions of the mesenteric lymph 
nodes and the spleen, 524. 

Secondary Lesions. The mouth, pharynx, parotid, pancreas, liver, and heart, 525. — 
Lesions in the blood-vessels, larynx, lungs, kidneys, ovaries, testicles, and brain, 
526. — Lesions in the muscles and skin, 527. — The bacillus of typhoid fever, 527. — 
Methods of staining the typhoid bacillus, 528.— Bibliography, 529. 

Typhus Fever, 530. 

Relapsing Fever, Lesions of various organs, 531. — Bacteria, 531, 532. 

Acute Cerebro- spinal Meningitis, 533. — Bacteria, 534. 

Diphtheria. Lesions, 535. — Bacteria found in diphtheria, 536. 

Asiatic Cholera. Lesions, 537, 538. — Bacteria, 538, 539, 540. 

Yellow Fever, 541. 

Tuberculosis, 542.— Tubercle bacilli, 545.— Methods of staining the tubercle bacilli, 
546. — Cultures of the tubercle bacilli, 547. 



X CONTENTS. 

Lupus, 548. 

Erysipelas, 550. — Streptococcus erysipelatos, 551. 

Pyaemia, 552. — Bacteria in pyaemia, 554. 

Anthrax, 555. — Bacillus anthracis, 556. 

Leprosy, 557. — Bacilli of leprosy, 558. 

Glanders (Farcy), 559. 

Hydrophobia, 561. 

The Malarial Feyers, 562. — Plasmodium malarias, 563. — Method of examining 
malarial blood, 564. 

Diseases Characterized by Alterations in the Composition of the Blood. 
Chlorosis, pernicious anaemia, Addison's disease, 565. — Leukaemia, pseudo- 
leukaemia, 567. 

Scorbutus, Purpura hemorrhagica, 568. 

ELematophilia, 569. 

Gout, 570. 

Diabetes, 571. 

Sunstroke, 572. 

Death prom Burning, 573. 

Death from Lightning, 574. 

Death from Suffocation, Asphyxia, 575. 

Death from Strangulation, Hanging, 516. — Death from Drowning, 577. 

Death from Poisoning. Sulphuric acid, 580. — Nitric acid, 581. — Hydrochloric 
acid, oxalic acid, tartaric acid; potash, soda, and their carbonates, 582.— Am- 
monia, potassium nitrate, phosphorus, 583. — Arsenic, 584. — Corrosive sublimate, 
lead, copper, 586. — Tartar emetic, vegetable irritants, cantharides, opium, 587. — 
Poisonous fungi, hydrocyanic acid, carbolic acid, alcohol, 588. — Chloroform, 
589. — Ether, chloral hydrate, strychnia, nux vomica, conium, aconite, bella- 
donna, lobelia innata, digitalis, stramonium, carbonic oxide, 590. — Carbonic acid, 
bibliography of poisons, 591. 



LIST OF ILLUSTEATIOWS. 



FIG. PAGE 

1. Side view of human brain, showing its fissures and convolutions, . . 11 

2. View of the base of the brain, with the temporal lobes turned backward 

and outward, 13 

3. Drawing of brain axis, separated from the brain mantle, ... 14 

4. Hyaline degeneration of capillary blood-vessels, 68 

■5. Coccidium oviforme, 70 

6. Cercomonas intestinalis, 71 

7. Trichomonas vaginalis, ........... 71 

•8. Distoma hepaticum, 71 

9. Head of Taenia solium, 73 

10. Head and proglottides of Taenia mediocanellata, 73 

11. Cuticula of echinococcus cyst, 74 

12. Scolices of Taenia echinococcus, 74 

13. Hooklets from scolex of Taenia echinococcus, 75 

14. Ascaris lumbricoides, 76 

15. Oxyuris vermicularis, 77 

16. Trichinae incysted in muscle, . . 78 

17. Filaria sanguinis hominis, . . . . . . . . . 80 

18. Sarcoptes hominis, 81 

19. Pediculus capitis, 81 

20. Actinomyces bovis, 84 

21. Drawing of three typical forms of bacteria, illustrating the three classes, 86 

22. Spheroidal bacteria, 87 

23. Bacilli in pairs, 88 

24. Bacilli in chains, 88 

25. Curved bacilli, forming spirals, 88 

26. Schematic drawing of spore-containing bacilli, 89 

27. Leptothrix buccalis, with micrococcus colonies, 90 

28. Spirillum serpens, 91 

29. Spirochsete denticola, 91 

30. Bacterial embolus in blood-vessels of the kidney in malignant endocar- 

ditis, 92 

31. Colonies of micrococci in a blood-vessel of the kidney causing abscess, . 93 

32. A potato culture, . 100 

33. A gelatin tube culture, 101 

34. A gelatin plate culture, 102 

35. Emigration of white blood-cells in inflamed frog's bladder, . . . 105 

36. Pus cells from catarrhal inflammation of bronchial mucous membrane, 106 

37. Croupous inflammation of trachea, 108 



xu 



LIST OF ILLUSTRATIONS. 



FIG. 

38. 
39. 
40. 
41. 
42. 
43. 
44. 
45. 
46. 
47. 
48. 
49. 
50. 
51. 
52. 
53. 
54. 
55. 
56. 
57. 
58. 
59. 
60. 
61. 
62. 
63. 
64. 
65. 
66. 
67. 
68. 
69. 
70. 
71. 
72. 
• 73. 
74. 
75. 
76. 
77. 
78. 
79. 
80. 
81. 
82. 
83. 
84. 
85. 



87. 



Granulation tissue from wound of skin, . 
Developing blood-vessels in new-formed tissue, 

Cicatricial tissue, 

Cellular peritonitis in dog, fourth day, . 

A tubercle granulum from the pleura, 

Diffuse tubercle tissue from acute phthisis, 

A miliary tubercle from a lymph gland, 

Dense fibroma of the abdominal wall, 

Myxoma of subcutaneous tissue, 

Myxoma in abdominal cavity, . 

Large spindle-celled sarcoma, . 

Small spindle-celled sarcoma, . 

Small round-celled sarcoma, 

Large round-celled sarcoma, 

Melano-sarcoma, 

Giant-celled sarcoma, 

Angio-sarcoma of liver, . 

Myxo-sarcoma of pharynx, 

Adeno-sarcoma of parotid, 

Endothelioma of dura mater, . 

Chondroma of subcutaneous tissue, 

Myxo-chondroma of cervical region 

Glioma of brain, 

Neuroglia or " spider " cells from glioma of brain, 

Myxoma of the uterus, . . . . 

Fibroma (false neuroma) of lumbar nerve, 

Multiple fibromata (false neuromata) of pneumogastric nerve 

Angioma telangiectoides of skin, 

Angioma cavernosa of liver, 

Congenital lymphangioma, 

Adenoma of mamma, 

Adenoma of the stomach, 

Cancer cells infiltrating the tissue near a tumor, 

Metastatic carcinoma in lymph vessels of the pleura 

Carcinoma uteri, showing pus cells, 

Epithelioma of the neck, . 

Epithelioma of axillary lymph node 

Epithelioma of back of hand, . 

A small epithelioma of the nose, 

Epithelioma of nose, 

Carcinoma mammae, scirrhus, . 

Medullary carcinoma of stomach, 

Colloid carcinoma of rectum, . 

Carcinoma myxomatodes mammae, 

Chronic pachymeningitis interna haemorrhagica 

Brain sand, 

Cellular meningitis, . . 

Acute purulent meningitis, .... 

Fatty degeneration of cells along blood-vessels of pia mater, after exuda 

tive meningitis, . 
A miliary tubercle of the pia mater, 



LIST OF ILLUSTRATIONS. Xlll 

FIG. PAGE 

88. A miliary tubercle of the pia mater, . 175 

89. Miliary tubercle of the pia mater undergoing cheesy degeneration, . 175 

90. Miliary tubercles of the ependyma, 175 

91. Miliary tubercle of the ependyma, 176 

92. Congenital hydrocephalus in child, 179 

93. Degenerated cells, cholestearin crystals, etc., from brain tissue in em- 

bolic softening of brain, . . . . . . . . . 182 

94. Blood-vessels from an area of embolic softening of brain, . . . 183 

95. Syphilitic obliterating endarteritis of a cerebral artery, .... 191 

96. Solitary tubercle of cerebellum, 192 

97. Descending gray degeneration, 200 

98. Ascending gray degeneration, 201 

99. Ascending gray degeneration, 202 

100. Degenerated tissue from acute myelitis, 203 

101. Poliomyelitis anterior, . . 204 

102. Poliomyelitis anterior, 204 

103. Posterior spinal sclerosis, 205 

104. Posterior spinal sclerosis, . . . 206 

105. Syringomyelia, . 208 

106. Hydromyelia, 209 

107. Multiple neuritis, 211 

108. An ulcer of the larynx in chronic catarrhal laryngitis, .... 215 

109. Tubercular laryngitis, 216 

110. Artificial pleurisy in dog, twenty-four hours' duration, .... 220 

111. Artificial pleurisy in dog on fifth day, 221 

112. Tubercular pleurisy, . . 225 

113. Acute catarrhal bronchitis, 227 

114. Section of the wall of a bronchiectasia, 230 

115. Emphysema, showing holes in the walls of the air vesicles, . . . 234 

116. Acute lobar pneumonia, pneumococci in the exudation, . . . 237 

117. Acute lobar pneumonia, with organized tissues in the air spaces, . . 239 

118. Pneumonia showing organized tissue in an air vesicle, .... 240 

119. Lobar pneumonia, with organized tissue in air vesicles ; blood-vessels 

injected, . . 241 

120. Broncho-pneumonia in a child, 243 

121. Broncho-pneumonia in an adult, . . . 244 

122. Persistent broncho-pneumonia, 245 

123. Lobular pneumonia in a child, complicating diphtheria, showing strep- 

tococci, 246 

124. The pneumonia of heart disease, 247 

125. Interstitial pneumonia, 248 

126. A miliary tubercle in the lung, 249 

127. A miliary tubercle, 250 

128. A miliary tubercle, 251 

129. Miliary tubercle in lung of child, showing tubercle bacilli, . . . 252 

130. An aggregation of miliary tubercles, 253 

131. Diffuse tubercular inflammation, 253 

132. An area of coagulation necrosis surrounded by a zone of pneumonia, . 254 

133. Tubercle tissue around an area of coagulation necrosis, . . . 255 

134. Chronic phthisis, 256 

135. Chronic phthisis, 257 



XIV LIST OF ILLUSTRATIONS. 

PIG. PAGE 

136. Chronic phthisis, 258 

137. Interstitial pneumonia of chronic phthisis, 259 

138. An old miliary tubercle converted into fibrous tissue, .... 260 

139. Interstitial syphilitic pneumonia, . . . 261 

140. Primary carcinoma of the lung, 262 

141. Fatty degeneration of the heart muscle, 275 

142. Fatty infiltration of the heart, 276 

143. Atrophic pericardial fat, . . . 277 

144. Vegetation on aortic valve in endocarditis, 278 

145. Mycotic endocarditis, . . . 279 

146. Chronic interstitial myocarditis, 281 

147. Chronic endarteritis, 286 

148. Chronic obliterating endarteritis, 286 

149. Atheroma of the aorta, 287 

150. Tubercular arteritis in the lung, . . . . . . . 289 

151. Tubercular phlebitis, . 297 

152. Acute inflammation of lymph node in typhoid fever, .... 302 

153. Chronic inflammation of bronchial lymph node, 303 

154. Pigmentation of bronchial lymph node, . . . . . . 304 

155. Diffuse sarcoma of the pharynx, . . . . • . . . . 319 

156. Acute cellular peritonitis, . . . 341 

157. Acute exudative peritonitis, , 342 

158. Chronic cellular peritonitis, . . 343 

159. Chronic peritonitis with adhesions, 344 

160. Section of a retro-peritoneal sarcoma, 348 

161. Chronic congestion of the liver, 352 

162. Fatty infiltration of liver cells, 356 

163. Amyloid degeneration of liver capillaries, 357 

164. Pigmentation of liver in malarial fever, 358 

165. Chronic interstitial hepatitis, 362 

166. Chronic interstitial hepatitis, ..." 364 

167. Syphilitic hepatitis, 366 

168. Gumma of the liver, 367 

169. Echinococcus multilocularis of the liver, . . . . . . 372 

170. Primary carcinoma of the common bile duct, 376 

171. Congestion of the spleen, 379 

172. Chronic indurative splenitis, 383 

173. Chronic interstitial splenitis, 384 

174. Malarial spleen, 384 

175. Fat necrosis in the pancreas, 391 

176. Atrophied thyroid in myxoedema, . 398 

177. Acute degeneration of the kidney, 404 

178. Acute nephritis, 405 

179. Acute nephritis with tuberculosis, . 406 

180. Acute nephritis, 407 

181. Acute diffuse nephritis, 408 

182. Chronic diffuse nephritis, . . . 412 

183. Waxy degeneration of vessels in kidney, 413 

184. Gonococci in pus cells, 429 

185. Chronic endometritis, 442 

186. Chronic endometritis, . . . 443 



LIST OF ILLUSTRATIONS. XV 

FIG. PAGE 

187. Uterine phlebitis, 446 

188. Adenomatous hyperplasia of uterine mucous membrane, . . . 447 

189. Carcinoma of cervix uteri, ulcerating, 451 

190. Chronic oophoritis, 454 

191. Chronic oophoritis, . 455 

192. Cystic adenoma of ovary, . . . . ' . . . . 457 

193. Fatty cells from an ovarian cyst, . . . . ' . . . . 458 

194. Suppurative mastitis 466 

195. Chronic inflammation of mamma, 467 

196. Intracanalicular fibroma of mamma, . 468 

197. Pericanalicular fibroma of mamma, . 469 

198. Chronic interstitial orchitis, 477 

199. Chronic orchitis, 478 

200. Rarefying osteitis, 487 

201. Condensing osteitis, . . . 489 

202. Tubercular osteitis, . . . . . 490 

203. Rachitic bone, 496 

204. Cells from marrow of femur in leukaemia, 498 

205. Chronic interstitial myositis, .511 

206. Progressive muscular atrophy, . . . . v . . . . 512 

207. Progressive muscular atrophy, 513 

208. Pseudo-hypertrophy of gastrocnemius muscle, 514 

209. Hyaline degeneration of muscle, 515 

210. Typhoid bacilli in the spleen, 527 

211. Typhoid bacilli from gelatin culture, 528 

212. Spirochete Obermeieri, 532 

213. Diphtheria of the trachea, 535 

214. Streptococcus diphtherias, 536 

215. Spirillum choleras asiaticse, . . . . 538 

216. Tubercle bacilli in sputum, . . . . . . . . 544 

217. Lupus of face, 548 

218. Micrococci in blood and lymph vessels of the skin in erysipelas, . . 550 

219. Streptococcus erysipelatos from culture, 551 

220. Micrococci in pyaemic pleurisy, 554 

221. Bacillus anthracis in liver of mouse, . 555 

222. Bacillus anthracis, 556 

223. Bacilli of leprosy, 557 

224. Plasmodium malarias, 563 



PART I. 



THE METHOD OF MAKING 



POST-MORTEM EXAMINATIONS 



AND OF 



PEESEEVIISTG DISEASED TISSUES. 



THE METHOD 



OF MAKING 



POST-MORTEM EXAMINATIONS. 



The particular object of making a post-mortem examination varies 
in different cases. It may be to determine whether a person has died 
from violence or poisoning; to account for a sudden death; or to study 
the lesions of disease. In any case the examination should embrace all 
the important parts of the body, not merely a suspected organ, and it 
should be recorded at the time it is made. 

In endeavoring to ascertain the cause of death, when the clinical 
history is imperfect or unknown, great care is necessary. Mechanical 
causes of death, which destroy life by abolishing the function of one of 
the important viscera, only occur in a moderate number of cases. Most 
of the lesions which we find after death rather indicate the disease than 
the cause of death. We do not know how great a degree of meningitis, 
or of pneumonia, or of endocarditis, or of cirrhosis, or of nephritis, 
necessarily causes death. On the contrary, we find that one patient 
recovers with an extent of lesion that is sufficient to destroy the life of 
another. So with accidents; there is often no evident reason why a frac- 
ture of the skull or of the pelvis should destroy life, but yet they usually 
do. In some of the general diseases, such as typhoid fever, the lesions 
cannot always be called the cause of death; in others, such as typhus 
fever, there may be no evident lesions at all. Sudden deaths of persons 
who have apparently been in good health up to the time of death are 
often particularly obscure. In many of them, we have to acknowledge 
that we can find no sufficient cause for the death. This is of course due 
to our imperfect knowledge. But it is much better in such cases to avow 
our ignorance than to attribute the death to some trifling lesion. The 
brain and the heart are the organs which are especially capable of giving 
symptoms during life without corresponding lesions after death. Very 
well-marked cardiac or cerebral symptoms may continue for days or 



4 THE METHOD OF MAKING 

months, and apparently destroy life, and yet after death we find no cor- 
responding anatomical changes. It is the novice in post-mortem exam- 
inations who is particularly apt to mistake ordinary post-mortem appear- 
ances for lesions. 

EXTEKNAL INSPECTION. 

Before commencing the examination of the internal viscera, it is al- 
ways necessary to make some inspection of the external surface of the 
body. The minuteness of this inspection will depend upon the charac- 
ter of the case: in the case of an unknown person, or of one suspected 
to have died from unnatural causes, it is necessary to search for and 
record, not only all contusions, wounds, etc., their size, situation, and 
condition, but also deformities from disease and any physical peculiari- 
ties of hair, eyes, teeth, moles, etc., by which the person may be identi- 
fied. In such cases it is well, if possible, to have a photograph taken of 
the entire body. In cases of doubtful identity, it is sometimes wise to 
make a wax or plaster cast of the outside of the teeth and jaws. In or- 
dinary examinations, we note the general nutritive condition of the body, 
and look for evidences of external injury, for skin diseases, ulcers, oedema, 
gouty deposits, abscesses, enlarged lymphatic glands, etc. The glans 
penis and prepuce are to be carefully searched for syphilitic cicatrices. 

It is usual to find certain changes in the external appearances of the 
body which are due to the cessation of life and the commencement of 
decomposition. We speak now of bodies which have not been buried, 
but which have been kept in the ordinary way, lying on the back and 
loosely covered with a shroud, or dressed with the ordinary clothes. 

Cadaveric Lividity. — After life becomes extinct and before the blood 
coagulates it settles in the veins of the more dependent parts of the body, 
producing, usually within a few hours after death, a mottling of the 
surface with irregular livid patches. These patches may coalesce, form- 
ing a uniform dusky red color over the back of the trunk, head, and ex- 
tremities, and sometimes over the ears, face, and neck. The same effect 
is observed on the anterior aspect of the body if it has lain on the face. 
At points of pressure, from folds in the clothes or from the weight of the 
body on the table, the red color is absent or less marked. These changes 
occur before putrefaction sets in. This cadaveric lividity or hypostasis 
should not be mistaken for ante-mortem ecchymosis, from which it may 
usually be readily distinguished by its position and extent, by the fact 
that the surface of the skin is not elevated, and by the fact that on in- 
cision no blood is found free in the interstices of the tissues. Not infre- 
quently the subcutaneous tissue in the vicinity of these post-mortem 
hypostases becomes infiltrated with reddish serum. Very soon after 
death, particularly in warm weather, the tissues immediately around the 
subcutaneous veins of the neck and thorax and in other situations may 



POST-MORTEM EXAMINATIONS. O 

become stained of a bluish-red color from the decomposition and escape 
from the vessels of the coloring matter of the blood. If the epidermis has 
been detached at any point, the skin beneath soon becomes dry and brown. 

Putrefactive Changes. — Usually in from one to three days, depend- 
ing upon circumstances, a greenish discoloration of the skin appears, at 
first upon the middle of the abdomen, over which it gradually spreads, 
assuming a deeper hue and often changing to a greenish purple or brown. 
Greenish patches may now appear on different parts of the body, earliest 
upon those overlying the internal cavities; this discoloration is probably 
produced by the action on the haemoglobin of gases developed by decom- 
position. The eyeballs now become flaccid, and if the eyelids are not 
closed the conjunctiva and cornea become brown and dry. The pres- 
sure of gases developed by decomposition in the internal cavities not in- 
frequently forces a greater or less quantity of frothy, reddish fluid or 
mucus from the mouth and nostrils, producing distention of the abdomen, 
and, if excessive, may produce changes of position of the blood in the ves- 
sels, and even a moderate amount of displacement of the internal organs. 

After five or six days, under ordinary circumstances, the entire sur- 
face is discolored green or brown. After this the epidermis becomes 
loosened from the formation of gases and separation of fluids beneath, 
and the tissues become flaccid. The abdomen and thorax may be 
greatly distended, the features distorted and scarcely recognizable from 
swelling, and the hair and nails loosened. Beyond this stage of putre- 
faction, the consecutive changes, leading to more or less disintegration 
of the soft tissues, can scarcely be followed with certainty. The rapid- 
ity with which these changes follow one another depends upon a variety 
of conditions, such as temperature, moisture, access of air, and the 
diseases which have preceded or caused death. Thus an elevated tem- 
perature, and the presence of air and moisture, hasten the advent and 
progress of putrefactive changes. The bodies of infants usually decom- 
pose more rapidly than those of adults, fat bodies more quickly than lean 
ones. The infectious diseases, intemperance, and the puerperal condition 
promote rapid decomposition; as does also death from suffocating gases. 
Poisoning by arsenic, alcohol, antimony, sulphuric acid, strychnine, and 
chloroform may retard the progress of decomposition. Burial in dry 
soil and submersion in water also retard the progress of decay. 

Cooling of the Body. — The internal temperature of the healthy living 
body is about 37.5° 0. (99.5° Fahr.). But it may be increased several 
degrees in consequence of disease. After death, the chemical changes 
upon which the maintenance of this temperature depends, rapidly 
diminish, and the body gradually cools to the temperature of the sur- 
rounding medium. This usually occurs in from about fifteen to twenty 
hours, but the time required depends upon a variety of conditions. 
Immediately after death, there is, in nearly all cases, a slight elevation 



6 THE METHOD OF MAKING 

of internal temperature, owing to the fact that the metabolic changes in 
the tissues still continue for a time, and the blood ceases to be cooled by 
passing through the lungs and peripheral capillaries. After death from 
certain diseases, yellow fever, cholera, rheumatic fever, and tetanus, a 
considerable elevation of internal temperature has been repeatedly ob- 
served. The time occupied by the cooling of the body may be prolonged 
after sudden death from accidents, acute diseases, apoplexy, and asphyxia. 
A number of cases are recorded in which the body retained its heat for 
several days without known cause. 

After death from wasting chronic disease, and in some cases after 
severe haemorrhages, the cooling of the body is very rapid, the external 
temperature being reduced to that of the surrounding air within four or 
five hours. Fat bodies cool less quickly than lean ones, the bodies of 
well-nourished adults less quickly than those of children or old persons. 
The temperature of the surrounding medium, the degree of protection 
of the body from currents of air, will, of couive, modify the progress of 
cooling; and the internal organs retain their heat naturally longer than 
the surface of the body. The rate at which cooling occurs is most rapid, 
as a rule, during the hours immediately following death, notwithstand- 
ing the post-mortem rise which may ensue. 

It will thus be seen that if required to pronounce upon the time which 
has elapsed since death in a given case, we can do so only approxi- 
mately. It is necessary to take into account all of the above-mentioned 
conditions which modify the rate of cooling of the body, and then we 
may be able to state only the probabilities of the case. It is furthermore 
unsafe in any case to infer the cause of death from the rate of cooling of 
the body. 

Rigor Mortis. — Death is usually succeeded immediately by a period 
of complete muscular relaxation; the jaw drops and the limbs become 
flaccid. The muscles may retain for two or three hours, however, the 
capacity of contracting on the applicatiou of appropriate stimuli. On 
the average within six hours the muscles become firm and rigid. This 
post-mortem rigidity is called rigor mortis. On the occurrence of the 
rigor mortis, the muscles become fixed in whatever position they may 
have had at the time of its occurrence. It usually begins in the muscles 
of the e3 r elids, extends to those of the back of the neck and lower jaw, 
then to the face and neck, and thence passing downward affects the 
muscles of the thorax and lower extremities. It usually disappears in 
the same order. Although commencing on the average six hours after 
death, it may set in almost instantly, or it may be delayed for twenty- 
four hours or more. It may pass off very rapidly, in rare cases in from 
one to three hours; or it may persist for two or three weeks or longer. 
It may be said in general that the average time of its disappearance is 
within twenty-four or forty-eight hours after its occurrence, depending 



POST-MORTEM EXAMINATIONS. 7 

on temperature, its intensity, the mode of death, the period of its 
advent, etc. Caspar states that in foetuses before term he has never 
observed rigidity, and that in young children it is feeble and of short 
duration. Its occurrence and phenomena may be in some cases of the 
highest medico-legal importance; but its careful observation does not, 
with our present knowledge of its significance, appear to essentially 
further the aims of the practical pathologist. 1 

Contusions. — It is often important to determine whether violence has 
been inflicted upon a body before death. In regard to this point, we 
must remember, first, that blows and falls of sufficient violence to frac- 
ture bones and rupture the viscera may leave no marks on the skin, even 
though the person has survived for several days; and, second, that there 
are post-mortem appearances which simulate ante-mortem bruises. A 
severe contusion during life may present, at first, no mark or only a gen- 
eral redness. After a short time, the injured part becomes swollen and 
of a red color; this color may be succeeded by a dark blue, and this in 
turn fade into a greenish yellow or yellow; these later appearances are 
due to an escape of blood from the vessels and to a subsequent decom- 
position of haemoglobin. If therefore we cut into such an ecchymosis 
after death, we find extravasated blood or the coloring matter of the 
blood, in the form of pigment granules, free in the tissues. Post-mor- 
tem discolorations, on the other hand, although their external appear- 
ance may resemble that of ante-mortem ecchymosis, are not formed by 
an extravasation of blood, but by a circumscribed congestion of the 
vessels, or by an escape of blood-stained serum. If we cut into such 
discolorations, therefore, we find no blood outside the vessels. 

Blows on the skin of a body which has not been dead for more than 
about two hours may produce true ecchymoses with extravasation of 
blood, such as can be distinguished with great difficulty or not at all 
from those formed during life. If putrefactive changes be present, the 
difficulty of distinguishing between ante-mortem and post-mortem bruises 
is greatly enhanced. 

Hanging and strangulation are attended with the formation of marks 
on the neck which are fully described in works on forensic medicine. 
These marks must not be confounded with the natural creases of the 
skin of the neck. Many adults during life have creases of the skin of 
the neck, one or more in number, running downward from the ear 
under the chin or encircling the neck. After death, these creases may 
be much more evident than during life, and may be rendered more de- 
cided by the position of the head and the freezing of the body. They 
regularly persist until the skin putrefies. 

1 For further details concerning rigor mortis, putrefactive changes, particularly 
the later stages, and the phenomena of cooling of the body, see Tidy, "Legal Medi- 
cine," vol. i., pp. 52-120, or other works on medical jurisprudence. 



8 THE METHOD OF MAKING 

Wounds. — We should notice the situation, extent, and direction of a 
wound; the condition of its edges and the surrounding tissues. If it be 
a deep, penetrating wound, its course and extent should be ascertained 
by careful dissection rather than by use of a probe. 

If the edges of a wound be inflamed and suppurating, or commencing 
to cicatrize, it must have been inflicted some time before death. In a 
wound inflicted a short time before death, the edges are usually everted; 
there may be more or less extravasation of blood into the surrounding 
tissues, and the vessels contain coagula; but sometimes none of these 
changes are observed. The chief characteristics of a wound inflicted 
after death are, absence of a considerable amount of bleeding, non-retrac- 
tion of the edges, and the absence of extravasation of blood into the tis- 
sues. But a wound inflicted within two hours after death may resemble 
very closely one inflicted during life. In general, unless a wound is old 
enough for its edges to present inflammatory changes, we must be very 
careful in asserting its ante-mortem or post-mortem character. 

Fractures. — It may be important to determine whether a bone was 
fractured before or after death. This point cannot always be decided. 
Fractures inflicted during life are, as a rule, attended with more extra- 
vasation of blood and evidences of reaction in the surrounding tissues; 
but fractures produced. within a few hours after death may resemble these 
very closely. Usually a greater degree of force is necessary to fracture 
bones in the dead than in the living body. 

Scars and Tattoo Marks. — The presence and character of cicatrices 
should be noticed. Scars produced by any considerable loss of substance 
may become very much smaller and less conspicuous, but never entirely 
disappear. Slight and superficial wounds, however, produce marks which 
may not be permanent. The discoloration produced by tattooing may, 
although rarely, disappear during life. 

INTERNAL EXAMINATION. 

After completing the external inspection of the body, we commence 
the internal examination. In order that this examination may be made 
both thoroughly and rapidly, we should follow a regular method. The 
method should be such as will enable us to examine the relations of parts 
to one another, without seriously disturbing them, and to remove and 
inspect the organs in such an order and manner as will not interfere with 
the examination of parts which are to follow. In certain cases it may 
be necessary to depart from the regular method; but, as a rule, the fol- 
lowing plan will be found most advantageous. 

It is important to remember the difference between the distribution 
of the blood in the body during life and after death. During life, the 
blood is in constant motion and is distributed in a regular way in the 
heart, capillaries, arteries, and veins. Inflammations and obstructions 



POST-MORTEM EXAMINATIONS. 9 

to the circulation may disturb this natural distribution and produce con- 
gestion of particular parts of the body. After death, the blood ceases 
to circulate; it leaves the left cavities of the heart, the arteries and ca- 
pillaries, and collects in the veins and the right cavities of the heart. 
According to the character of the disease which causes death, coagula- 
tion of the blood takes place more or less extensively and at an earlier or 
later period. The local congestions which existed during life often dis- 
appear after death. On the other hand, local congestions are found 
after death which did not exist during life. Thus, after death, the scalp 
often contains a large amount of venous blood. The veins of the pia 
mater and the sinuses of the dura mater may be filled with blood. The 
mucous membrane of the larynx and trachea may appear to be deeply 
congested. The lungs are congested if the patient has been comatose 
for some hours before death. All the tissues of the back and the mem- 
branes of the spinal cord are often gorged with venous blood. The right 
auricle and ventricle of the heart may contain fluid or clotted blood in 
considerable quantity. 

THE HEAD. 

The scalp is divided by an incision across the vertex from ear to ear. 
The flaps are dissected forward and backward, taking up the temporal 
muscles with the skin, and leaving the pericranium attached to the bone. 
The internal surface of the scalp and the pericranium are to be searched 
for ecchymoses and inflammatory lesions. A circular incision is then 
made with a saw, and the roof of the cranium removed. The incision 
in front should pass through a point about three and one-half inches 
above the bridge of the nose, behind through the occipital protuberance. 
When the roof of the cranium is thus entirely loosened, a stout hook is 
introduced under the upper edge of the calvarium, and this is wrenched 
off with a jerk. 

Sometimes the dura mater is so adherent to the calvarium that the 
latter cannot be torn from it without injury to the brain. In this case, 
the dura mater may be cut through at the level of the cranial incision, 
and the brain removed with the calvarium and separated afterwards. 
Or, which is better, after the circular incision has been made through 
the bone, a longitudinal incision is made, from front to back, about 
three-quarters of an inch to one side of the median line of the skull, and 
a segment of bone removed. The knife blade may now be inserted from 
the open side, and the dura cut away from the skull cap along the line 
of the longitudinal sinus, where the adhesions are apt to be most firm. 

We should notice whether or not the calvarium is symmetrical. The 
cranial bones increase in size by a growth of bone at the edges of the su- 
tures. If any suture become completely ossified and closed prematurely, 
the bones will be unequally developed. The thickness and density of 
the cranial bones vary considerably within the limits of health. There 



10 THE METHOD OF MAKING 

are often deep depressions on the inner surface of the skull along the 
sagittal suture, caused by the pressure of the Pacchionian bodies, and of 
no pathological significance. We should observe the blood content of 
the bone, determine the existence or absence of fractures, inflammatory 
lesions, exostoses, etc. 

The Dura Mater is now exposed to view. It will be found more or 
less adherent to the calvarium; a moderate amount of adherence, espe- 
cially in old persons, does not denote disease. Very extensive and firm 
adhesions are usually produced by inflammation. Near the median line, 
the Pacchionian bodies often project through the dura mater and may 
produce indentations in the internal surface of the calvarium. We must 
look for clots and for tumors and for inflammatory lesions on the exter- 
nal surface of the dura mater. The longitudinal sinus should be laid 
open and its contents examined. A circular incision is then made 
through the dura mater in a line corresponding to the cranial incision; 
the falx is divided between the anterior lobes of the brain, and the en- 
tire membrane drawn back. We should observe the existence of abnor- 
mal adhesions of the dura mater to the pia mater, bearing in mind that 
a moderate amount of adhesion along the longitudinal fissure is normal. 
The internal surface of the dura mater is to be examined for the pro- 
ducts of inflammation and for tumors. 

The Pia Mater covering the convex surface of the brain is now ex- 
posed. The degree of congestion, and the existence of serum, pus, or 
blood, beneath, within, or upon it, are now to be ascertained before the 
brain is removed. The pia mater in old persons frequently loses its 
transparency and becomes thick and white; this change is most marked 
along the longitudinal fissure and large vessels. Marked and general 
thickening of the pia mater is produced by chronic inflammation. Along 
the longitudinal fissure, and sometimes at a considerable distance from 
it, we usually find small elevated whitish nodules, which are the Pac- 
chionian bodies and are normal in the adult. 

The amount of serum beneath the pia mater varies. A considerable 
amount, especially in cachectic persons, may exist without brain disease. 
Clear serum raising the pia mater and separating the convolutions of the 
brain may be simply dropsical or due to chronic meningitis. Turbid 
and purulent serum, beneath and in the pia mater, is produced by 
acute or chronic meningitis. The degree of flatness of the surface of the 
convolutions should be observed before removing the brain; for, when 
marked, it affords an important indication of pressure, from haemorrhage, 
inflammatory products, internal fluid effusions, and tumors. The pia 
mater should be carefully examined for miliary tubercles. 

The Brain. — After examining the convex surface of the brain, the 
anterior lobes of the cerebrum are to be pulled gently backward, the 
nerves, vessels, and tentorium severed, and the medulla cut across as low 



POST-MORTEM EXAMINATIONS. 



11 



down as possible. The brain is now removed from the cranium by pass- 
ing the fingers of one hand down, beneath and behind the lobes of the 
cerebellum, and drawing the brain out, supporting the convexity with 
the other hand. 

The adult brain in the male weighs on the average about 1,400 gm. 
(49^- oz.); that of the female, about 155 gm. (5 oz.) less. The average 
proportional weight of the brain to that of the body is about one-forty- 
fifth, although in this, as in the absolute weight, there is considerable 
variation. 

The exact situation of any lesion which is apparent externally, should 
be described by its relation to the lobes, fissures, convolutions, and sulci. 




Fig. 1.— Side View of the Human Brain, showing its Fissures and Convolutions. 



The brain is first laid upon its convex surface, and the anterior, mid- 
dle, and posterior cerebral arteries, as well as the basilar and the caro- 
tids, are to be examined for emboli, thrombi, atheroma, and aneurisms. 
Evidence of extravasations of blood, tumors, and inflammatory lesions 
are now to be looked for. The brain is next turned over on to its base. 
An incision is made through the pia mater over the convex surface of 
the cerebrum. The membrane is stripped up, and its adherence to the 
brain and its thickness noted. 

The more common method of opening the brain is as follows: the 
halves of the cerebrum are to be separated until the superior surface of 
the corpus callosum is exposed. A longitudinal incision is made through 
the junction of the corpus callosum and the cerebrum, and downward 
into the ventricle. The incision should be made carefully, so as not to cut 



12 THE METHOD OF MAKING 

through the ventricle into the ganglia below. The incision thus made 
through the roof of the ventricle is prolonged backward and forward in 
the direction of the cornua, so as to expose the entire ventricle. A longi- 
tudinal incision is then made outward and backward into the hemisphere, 
from the outer edge of the lateral ventricle, nearly to the pia mater. A 
second incision is then made through this cut surface outward, and this 
is repeated until the hemisphere is divided into a number of long, prism- 
shaped pieces, held together by the pia mater and a small portion <3f the 
cortex. The brain is now turned around so as to bring the other hemi- 
sphere under the hand, and the operation is repeated on the other side. 

The size, shape, and contents of the ventricles should be noticed, and 
the thickness and appearance of the ependyma. 

The fornix and the central portion of the corpus callosum are cut 
across by passing the point of the knife through the foramen of Munro 
and cutting upward. They are then drawn backward, one of the poste- 
rior cornua of the fornix being severed and laid to one side. The velum 
interposifeum and the choroid plexus are now dissected up, the blood con- 
tents and the general appearance noted, and the third ventricle examined. 
Not infrequently small cysts of the choroid are found, which seem to 
have little or no pathological significance. 

The fourth ventricle is now opened by a longitudinal incision through 
the vermiform process. Each hemisphere of the cerebellum is divided 
first into two parts by an incision through the upper and inner convex 
border, and then each segment is further divided by incisions in the same 
direction. 

Thin transverse sections are now made through the cerebral ganglia, 
commencing in front. The ganglia are supported, and the sections 
caused to fall apart as they are cut, by carrying the fingers of one hand 
under the brain, and gently lifting the ganglia at points just beneath 
where the sections are made. It is important to observe the exact posi- 
tion of any lesion which may be discovered in the cerebral ganglia, their 
relations to the external and internal capsule, and to the caudate and 
lenticular nucleus. 

Finally the segments of the cerebrum and cerebellum are folded up 
together into their original positions, the whole is turned over on to the 
vertex, and thin sections are made through the medulla. Small clots in 
the medulla should not be overlooked. 

In case of the discovery of apoplectic clots, areas of softening, etc., 
either in the hemispheres or in the basal ganglia, after their location and 
extent is determined, they should be carefully searched for lesions of 
the blood-vessels, minute aneurisms, areas of degeneration, and ruptures. 
For this purpose it may be necessary to allow a stream of water to run 
over the affected portion, so as to wash out the brain substance and 
expose the vessels. In some cases the blood-vessels are best exposed by 



POST-MOBTEM EXAMINATIONS. 



13 



macerating the brain tissue at the seat of the lesion for some hours in 
water, and then washing out the brain substance under the faucet. 

While the above mode of dissecting the brain gives a very complete 
view of the seat and extent of lesions in general, where a more exact lo- 
calization of lesions with a microscopical examination is to be made the 
following is a better method of opening the brain: 

After completing the external examination, as detailed above, the 
brain is laid on its vertex, the cerebellar end towards the operator. The 
cerebellum is raised by the fingers of the left hand, and the pia cut 
through along the sides of the corpora quadrigemina and along the 
inner margin of the temporal lobes to the middle cerebral artery on 
both sides. Then, raising the temporal lobes, in turn, by their apices, 
the pia is cut through along the course of the middle cerebral artery 
into the Sylvian fissure, and along the course of its posterior branch to 
its end. Now drawing the temporal lobes one after the other upward 
and outward, their junction with the base is cut, the knife being held 
horizontally so as not to injure the basal ganglia, until the descending 
horn is opened. The point of the knife being in the descending cornua, 
the incision through the brain substance then passes outward and back- 
ward well into the posterior cornua, thus partially severing, at the lateral 
surface of the brain, the junction of the occipital and temporal lobes. 
The temporal lobes are then turned outward and backward (Fig. 2). 




Fig. 2.— View of the Base of the Brain, with the Temporal Lobes turned Backward 
and Outward. 

A, B. Line of transverse incision. 

The operculum is now pulled well outward, completely exposing the 
island of Reil, and a slightly curved transverse incision is made, deep 
enough to pass into the anterior horns of the ventricles, connecting the 
anterior sulci of the island of Reil (Fig. 2, A, B). 



14 THE METHOD OF MAKING 

Now raising the cerebellum and inserting the point of the knife into 
the ventricle, with short incisions from within outward cut through the 
internal capsule on either side from back to front, care being taken not 
to injure the basal ganglia. Then cut across the crura of the fornix and 
the septum lucidum, leaving the fornix lying on the corpus callosum. 

The square basal piece thus freed — the brain axis — includes the 
island of Keil, the basal ganglia, the crura, pons, medulla, and cerebel- 
lum (Fig. 3). 




Fig. 3.— Drawing of the Brain Axis, separated from the Brain Mantle, as seen from 
above. 

The remaining portion — the brain mantle — includes the convolutions, 
corpus callosum, and fornix. 

The basal piece may be further examined by a series of transverse 
incisions from one-half to three-quarters of an inch apart, and it may 
then be hardened either with or without the cerebellum. The convolu- 
tions may be cut into small pieces by longitudinal and transverse inci- 
sions, made from within and not reaching quite to the pia mater, which 
will then serve to hold the pieces together in their proper relations to 
one another. 1 

For the methods of hardening and preserving the brain tissues, see 
p. 15. 

The Base of the Cranium. — We now return to the skull. The re- 
maining sinuses of the dura mater should be opened, and this membrane 
then entirely stripped from the bone. The bones at the base of the 
skull are to be examined for fractures, inflammatory lesions, and tumors. 
In cases of acute purulent meningitis, the temporal and frontal bones 

1 For further details of this method of opening the brain and a consideration of its 
advantages, see Van Gieson, New York Medical Journal, July 20th, 1889. 



POST-MORTEM EXAMINATIONS. 15 

should be carefully examined, as the inflammatory process is sometimes 
transmitted from the internal ear, or mastoid cells, or frontal sinuses. 

The eyes may be removed by breaking the roof of the orbit with a 
hammer, removing the fragments of bone, and dissecting away bone 
and muscles, so as to expose the optic nerve and posterior segment of 
the eye. That portion of the globe which is not covered by conjunctiva 
can now be cut away with scissors, and removed with the optic nerve, 
or, when permissible, the whole eye may be cut out. 

Hardening and Preservation of the Tissues for Microscopical Examination. — For 
the study of tumors and inflammatory lesions of the bones of the skull and ossifica- 
tions of the dura mater and pia mater, the affected portions should be cut into small 
pieces, decalcified with picric acid, and subsequently hardened in strong alcohol. In 
the ordinary lesions of the dura mater, the tissues are best hardened and preserved by 
stretching the diseased portions on a flat piece of wood or cork with pins, and placing 
them in Miiller's fluid. 1 

The pia mater is so delicate that if it be torn from the brain when quite fresh, its 
tissues are apt to be injured. The portions of the pia mater which are to be preserved 
should therefore be removed by cutting off slices of the brain substance about one-half 
an inch thick, with the membrane still attached, and placing the whole in Miiller's 
fluid. After twenty-four hours the pia mater will have become sufficiently hard to per- 
mit of its being stripped off without injury, and it is then spread loosely on a flat cork 
with pins, the free surface outward, and the cork floated, specimen side down, in a dish 
of alcohol (80 per cent). The next day strong alcohol may be used, and the harden- 
ing is complete in three or four days. The pia mater should not remain longer than 
twenty-four hours in Miiller's fluid before being stripped off; for after this time it 
usually becomes so firmly attached to the brain substance as to render its removal very 
difficult. 

The ependyma, when this alone is to be studied, may be sliced off with a sufficient 
quantity of underlying brain substance to prevent its folding, and hardened in Miiller's 
fluid. Special care should be exercised not to touch the surface of the ependyma, 
since the epithelium is easily rubbed off. 

The brain substance, after having been cut into sufficiently small pieces for the 
general examination, should be hardened in Miiller's fluid. Large quantities of the 
fluid should be used, four or five times the bulk of the tissue, and the pieces of tissue 
should either be suspended in gauze or kept apart by a little absorbent cotton. The 
fluid should be kept cool, and changed on the second, fifth, and eighth days, and again 
in the third week. 

In general, two or three months are required to secure a good hardening with 
Miiller's fluid. When the hardening is complete, the brain tissue is rinsed off with 
water and put in eighty-per-cent alcohol, in which it may be kept, preferably in the 
dark. 

Great care is required in hardening and preserving nerve tissues, and most of the 
ordinarily practised methods give only caricatures and gross distortions of the brain 
structure. 

Too long a soaking in Miiller's fluid renders brain tissue very brittle. To get the 
best hardening, the single pieces ought not to be larger than 1 c.c. 

*For the details of the methods of hardening, decalcifying, staining, etc., see the 
end of Part I. 



16 THE METHOD OF MAXING 

Certain lesions, particularly the softenings of the brain, are best studied by teasing, 
when fresh, in one-half-per-cent solution of sodium chloride, or in frozen sections of 
the fresh tissue. (See chapter on the Nervous System.) The blood-vessels should be 
stretched on cork with pins, and hardened with Miiller's fluid and alcohol. The eye 
and portion of the optic nerve, if removed, should be hardened with Miiller's fluid. 1 

THE SPINAL COED. 

The examination of the spinal cord is usually most conveniently 
made after the removal of the brain. 

The body should be placed face downwards, with a block under the 
thorax and the head hanging over the edge of the table. An incision is 
made through the skin and muscles along the entire length of the spine, 
and the soft parts dissected away on each side so as to expose the laminae 
of the vertebral column. The laminae are then divided close within the 
articular processes, with the rachitome or with the saw and chisel. The 
spinous processes and laminae are then torn away together with a stout 
hook, and the cord is thus exposed. 

The saw should be so directed in severing the laminae that the 
incision shall touch the outer border of the spinal canal, as otherwise the 
laminae and spinous processes are not easily removed. 

By means of a long, curved chisel, made for this purpose, the bodies 
of the vertebrae may be removed from the front after the thoracic and 
abdominal viscera are taken out, and the cord thus exposed and re- 
moved. 

When the body has lain on the back, the membranes of the cord may 
be found considerably congested without indicating the pre-existence of 
any disease. If the body has lain for some time, especially in warm 
weather, serous fluid may have accumulated within the membranes as a 
result of post-mortem change. 

The roots of the nerves are now to be cut across, as far away as 
possible from the cord, and the cord removed in its membranes, care 
being taken not to press it in any way. It is the safest plan not to 
grasp the cord itself, but with a forceps to seize the dura mater and 
thus lift it up at once as it is freed from its attachments. It is now laid 
on the table, and the dura mater laid open with scissors on the ante- 
rior and posterior surfaces over its entire length, and searched for tumors, 
inflammatory lesions, etc. The finger should be passed gently along the 
cord as it lies on the table, so as to detect any marked softening or scle- 
rosis. It should now be held lightly over the fingers, and smooth trans- 
verse incisions made, with a very sharp knife, about one-half an inch 
apart through its entire substance, leaving the segments attached to the 
pia mater. The cut surfaces should be carefully examined for abnormal 

1 For further details of the methods of dissecting, hardening, and preserving the 
brain and spinal cord, consult Van Gieson, loc. cit. 



POST-MORTEM EXAMINATIONS. 17 

blood contents, haemorrhages, inflammatory lesions, softening, scleroses, 
and pigmentations. Important lesion of the cord may be invisible to 
the naked eye, and hence, if disease be suspected, the organ should be 
preserved for microscopical examination. After removal of the cord, 
fractures and displacements of the vertebrae are easily recognized. 

Preservation of the Spinal Cord and its Membranes, and of Peripheral Nerves. — The 
entire cord, with its nerve roots and dura — the segments into which it has been cut for 
gross examination being left in place — should be laid or suspended in a large jar of 
Mtiller's fluid, the segments slightly separated from each other by a little absorbent 
cotton. 

The hardening and preservation of the cord should be done by the same method as 
suggested above for the brain. The same care should be exercised as in the brain 
not to permit the cord to become brittle by remaining too long in the Miiller's fluid. 
If the dura mater of the cord alone is to be preserved, it should be treated in the 
manner suggested for the dura mater cerebralis. The pia mater spinalis is best 
studied in sections through the entire cord, the membrane being left in situ. 

Peripheral nerves may be hardened in Miiller's fluid, care being taken that they do 
not become brittle by too long soaking in it. The hardening is completed and the 
specimen preserved in alcohol. 

For the hardening of the peripheral nerves, osmic acid is very useful, especially 
when changes in the myeline are to be sought after. 

As osmic acid does not readily penetrate the lamellar sheath so as to come in con- 
tact with the nerve fibres, in trunks of any considerable size, the following procedure 
as suggested by Van Gieson will be found useful: A piece about one-half inch long is 
cut .from the nerve to be examined, and, seizing one end of this segment with a 
forceps, with another forceps the individual nerve fibres, or small clusters of these, 
are pulled out of the lamellar sheath and put at once in one-per-cent aqueous solution 
of osmic acid, in which they remain twenty-four hours, and are then washed and 
transferred to glycerin, to which twenty-five per cent alcohol is added. In this mix- 
ture they may be preserved. 

THE THORAX AND ABDOMEN. 

To examine these cavities, the body is replaced on its back, and a 
single straight incision is made from the top of the sternum to the pubes, 
passing to the left of the umbilicus. For this purpose a large knife 
should be used, held firmly in the whole hand, and the movement should 
be mainly from the shoulder. The first incision should divide every- 
thing down to the sternum and peritoneum. A short incision should 
then be made through the peritoneum, just below the ensiform cartilage. 
Into this opening two fingers of the left hand are introduced and 
separated from one another, and, the parietes being raised and the sides 
of the opening being held apart by the fingers, the peritoneum is divided 
to the pubes, care being taken to hold the knife horizontally so as not to 
cut the intestines. The skin and muscles are then dissected off from the 
thorax on both sides as far back as the false ribs. 

This dissection should be made by long sweeps of the knife, which 
should be made to cut with the full blade and not with the point only; 
2 



18 THE METHOD OF MAKING 

and if the skin and muscles be pulled strongly away from the chest with 
the left hand, it may be done very rapidly and with a few strokes of the 
knife. We notice here the amount of subcutaneous fat and the con- 
dition of the muscles. In order better to expose the abdominal cavity, 
the rectus abdominis muscles should be divided transversely beneath the 
skin just above the pubes, and the abdominal flaps may then be turned 
freely outward. 

General Inspectioyi of the Abdominal Cavity. — We first notice the 
position and general condition of the viscera. It is best at this stage of 
the examination to note the condition of the vermiform appendix, and 
to look over the peritoneal cavity for serum, inflammatory lesions, evi- 
dences of perforation, and for the existence of invagination, incarceration, 
and herniae of the intestines. A small quantity of reddish serum is fre- 
quently found in the abdominal cavity, particularly in warm weather, as 
the result of commencing decomposition. 

It should be remarked here that a variety of striking changes in the 
character and appearance of the internal organs are produced by putre- 
faction — changes which are often mistakenly regarded as evidences of 
disease, and much experience is required in judging correctly of their 
significance. These changes are, in general, softening and discoloration, 
both of which may occur as the result of disease. It may be said in 
general that the post-mortem reddening or hypostases are most marked 
in the more dependent parts of the organs. Post-mortem softening 
usually affects entire organs, not being limited to a part, as is often the 
case in disease. Gray or greenish-brown post-mortem discolorations are 
apt to appear in those organs or parts of organs which lie in contact with 
the intestinal canal. Parts of internal organs, such as the liver, which 
have been the seat of localized congestion during life, may after death 
take on a dark greenish color. 

The omentum is usually spread over the surface of the small intes- 
tines, but it may be rolled up and displaced in a variety of ways, or may 
be adherent at some point to the small intestines or the abdominal wall. 
The surface of the small intestines should be smooth and shining. 
They may be greatly distended with gas, and thus so completely cover 
the abdominal viscera that it becomes necessary to let out some of the 
gas by a small puncture. The transverse colon passes across the abdo- 
men through the upper part of the umbilical region. It may be lower 
than the umbilicus or higher up against the liver and diaphragm; it may 
be distended with gas or contracted. 

The liver is situated in the right hypochondriac and epigastric re- 
gions, filling the concavity of the diaphragm. Its upper border reaches, 
in the linea mammilaris, to the fifth intercostal space; in the linea 
axillaris, to the seventh intercostal space; close to the vertebral column, 
to the tenth intercostal space. At the median line the upper border of 



POST-MORTEM EXAMINATIONS. 19 

the liver corresponds to the lower border of the heart. The left lobe 
extends about three inches to the left of the median line. The lower 
border of the right lobe usually reaches to the free border of the ribs, 
while the left lobe is visible for about an inch below the ensiform car- 
tilage. In women, the liver is usually lower than in men. 

The position of the liver is affected by changes in the thoracic cavity, 
forcing it downward; by change in the abdominal cavity, forcing it up- 
ward; by constriction of the waist in tight lacing, forcing it either up- 
ward or downward; by changes in the size of the organ itself. The liver 
may not only be displaced downward but dislocated, so that its convex 
surface faces the abdominal wall, and its posterior edge is turned up- 
ward against the diaphragm. 

The stomach is situated in the left hypochondriac and epigastric 
regions, extending also into the right hypochondrium; it lies in part 
against the anterior wall of the abdomen, in part beneath the liver and 
diaphragm, and above the transverse colon. Its anterior surface, which 
is directed upward and forward, is in contact above with the diaphragm 
and the under surface of the liver, and lower down with the abdominal 
wall opposite to the epigastric region. Its posterior surface is turned 
downward and backward, and rests on the transverse mesocolon, the 
pancreas, and the great vessels. To its lesser curvature or upper border 
are attached the gastro-phrenic ligament and the gastro-hepat ; c omen- 
tum. To the greater curvature or lower border is attached the gastro- 
colic omentum. Its cardiac orifice communicates with the oesophagus, 
its pyloric end with tue duodenum. 

When the stomach is distended, the greater curvature is elevated and 
carried forward, the anterior surface is turned upward and the posterior 
surface downward. When distended with food or gas, the organ is 
prominent; when empty, it may hardly be visible below the ribs; when 
the intestines are dilated, it may be entirely covered by them. 

Before opening the thorax, the hand should be passed up against the 
under surface of the diaphragm on either side to determine its height. 
According to Quain, the vault of the diaphragm rises, in the dead body, 
on the right side to the level of the junction of the fifth rib and sternum, 
on the left side as high as the sixth rib. Both the relative and the ab- 
solute height of the diaphragm vary under a variety of pathological con- 
ditions. 

If the existence of air or gas in the pleural cavities be suspected, the 
abdomiual cavity should be filled with water and the diaphragm punc- 
tured below the level of the fluid. If air be present, it will escape in 
bubbles through the water. 



20 THE METHOD OF MAKING 

THE THORAX. 

We now leave the abdominal viscera and proceed to the examination 
of the thorax. With a costatome or a strong knife, the costal cartilages 
are divided close to the ribs, the clavicles are disarticulated from the 
sternum, and the latter removed, taking care not to wound the large 
veins. We first examine the position of the heart and lungs. 

The Heart. — The upper border of the heart is on a level with the 
third costal cartilage; the lower border extends from 1.3 cm. (% in.) be- 
low the lower end of the sternum to the fifth left intercostal space. The 
left boundary of the heart is situated to the left of the junction of the 
fifth rib with its costal cartilage, and behind or to the left of a vertical 
line drawn downward from the left nipple. The right boundary ex- 
tends about 2.5 cm. (1 in.) to the right of the right edge of the ster- 
num. The portion of the heart uncovered by the lungs is of an irregu- 
lar quadrangular shape. Its lateral diameter is from 3.8 cm. to 11.1 
cm. (1^-44 inches); its upper boundary varies from the level of the 
second left costal cartilage to that of the fifth, but it is usually behind 
the third or fourth cartilage or fourth space. ^ 

The area of the heart which is found uncovered will, however, vary 
much according to the degree to which the lungs collapse after opening 
the chest. Any disease which diminishes the size of the lungs, or pleu- 
ritic adhesions which retract or bind them down, may increase the area 
of exposed heart. On the other hand, emphysema, pneumonia, or any 
disease which increases the size of, or retains the air in, the lungs, may 
diminish the area of exposed heart. The exposed area varies also with 
the size of the heart itself. 

The Pericardium is now opened by a slightly oblique incision on 
its anterior surface. The existence of serous, fibrinous, or purulent exu- 
dation, and of adhesions, is to be noticed. A small quantity of clear 
serum exists normally in the pericardial sac, and this serum may be 
blood-stained from beginning decomposition. White thickenings of the 
pericardium on the surfaces of the heart are often seen; they do not 
indicate any important disease. 

Now that the pericardial sac is open, the position of the heart can be 
clearly seen. It lies obliquely in the chest, its long axis at an angle of 
about 60 degrees with that of the thorax. The portion of the heart 
which is first seen is the anterior surface of the right ventricle; upward 
and to the right of this is the right auricle, which lies about two-thirds 
on the right of the sternum and about one-third behind it. Its upper 
border usually corresponds to the plane of the middle of the anterior 
end of the second intercostal space on the right side. Its size varies 
with the amount of blood which it contains. The left auricle lies 
behind the root of the pulmonary artery, so that only its appendix is 



POST-MORTEM EXAMINATIONS. 21 

visible. The middle of the auricle corresponds to the third costal car- 
tilage. Of the left ventricle only a narrow rim is seen, on the left 
side of the right ventricle. The pulmonary valve is usually entirely or 
in part on the left side of the sternum behind the second space or third 
costal cartilage. 

The aortic valve is usually at the level of the third cartilage or the 
third space, and behind the left two-thirds or half of the sternum. The 
mitral valve is oblique, the upper end to the left. It is on the level of 
the third to the fourth cartilage near the middle of the sternum. The 
tricuspid is oblique, its upper end to the left; the upper end is at the 
level of the third cartilage, the third space, or the fourth cartilage. The 
valve is opposite to the middle of the sternum. 

The hand should now be passed over the arch of the aorta, to ascer- 
tain whether or not an aneurism is present. The heart is then grasped 
at the apex, raised out of the pericardium, tilted upward and removed 
unopened by cutting through the vessels at its base. 

To determine the sufficiency of the aortic and pulmonary valves, the 
heart is held horizontally by both auricles, so as not to pull the valves 
open, and water is poured into the aortic and pulmonary arteries, and 
we observe how well the valves support the column of liquid. To ascer- 
tain the sufficiency of the mitral and tricuspid valves, the auricles are 
first laid open so as to expose the upper surfaces of the valves. A large 
pipe is passed through the aorta or pulmonary artery beyond their valves, 
and a small stream of water allowed to flow into the ventricles. The 
auriculo-ventricular valves will be swollen upward, and we can observe 
their degree of sufficiency. The tricuspid valve is normally somewhat 
insufficient. These water tests, however carefully applied, are not very 
reliable, since under the most favorable conditions the natural bearings 
of the valves are not perfectly preserved. 

To ascertain the size of the different valvular openings, we introduce 
the fingers, held flat with their sides in contact, into each of the orifices, 
and then measure the width of the fingers at the point where they fill 
the orifice. In this way we find that, under normal conditions in the 
adult, the aortic orifice measures about 2.5 cm. (1 in.), the mitral 
valve about 4.5 cm. (1.8 in.), the pulmonary about 3.1 cm. (1.2 in.), 
the tricuspid about 5 cm. (2 in.). 

In order to examine the interior of the heart, we first make an inci- 
sion through the anterior wall of the right ventricle, close to the septum, 
and reaching to the apex of the ventricle ; through this opening the 
blade of the enterotome is passed into the pulmonary artery, and the 
ventricle and artery laid open. With a little care, the incision may be 
made to pass through one of the points of junction of the valves. 

The auricles and ventricles may be empty, or may contain fluid blood, 
or the so-called heart-clots. These heart-clots are of two kinds — those 



22 THE METHOD OF MAKING; 

which are formed some time before death, and those which are formed 
during the last hours of life and after death. The clots which are 
formed some time before death are usually associated with organic dis- 
ease of the heart, especially with dilatation of the ventricles. They are 
firm, dry, and of whitish color ; they may soften or be infiltrated with 
the salts of lime. They are free in the cavities of the heart, or entangled 
in the trabecule, or firmly adherent to the endocardium. They are com- 
posed of coagulated fibrin, or, rarely, of sarcomatous tissue as a compli- 
cation of sarcoma in other parts of the body. The clots which are 
formed during the last hours of life and after death are red, yellow, or 
white. They may be soft or succulent, or quite firm. They may be 
free in the heart cavities, or be adherent to the trabecule, or extend 
into the large vessels. They are usually most constant and of largest 
size in the right auricle and ventricle. Such clots may be formed within 
two hours after death. Clots of this character are a regular post-mortem 
condition, and of no pathological significance. It is evident, however, 
if the blood did coagulate in the heart within twenty-four hours before 
death, that this coagulum could not be distinguished from the ordinary 
post-mortem clots. If it is supposed, therefore, that a person dies from 
heart-clot developed a few hours before death, the proof of this must be 
derived from the clinical symptoms, and not from the autopsy. 

The condition of the pulmonary valves and of the endocardium, and 
the thickness and appearance of the walls of the ventricle, are now noticed; 
the left ventricle is opened by an incision through its anterior wall, 
close to the septum, and examined in the same way. We sometimes see 
the endocardium of the upper part of the left ventricle thick and white 
without the existence of valvular lesions or any clinical history of disease. 
The endocardium and valves are often stained red, particularly in warm 
weather, by imbibition of coloring matter of the blood set free by decom- 
position. To complete the examination of the cavities, the enterotome 
is passed into each auricle, carried down into the corresponding ventricle, 
and an incision made along the outer border of both auricle and ventricle 
to the apex of the latter. In this way the auriculo-ventricular valves are 
completely exposed. 

After removing the blood, the heart should be finally weighed. In 
adults, the normal average weight of the heart is about 337 gm. (about 
12 oz.). The relative weight of the heart to that of the body is in males 
about 1 : 158-178 ; in females, about 1 : 149-176. According to Buhl, 
the average thickness of the wall of the left ventricle at about the middle 
of the cavity is from 1.6 cm. to 1.7 cm. (from about | to -f in.); of the 
right ventricle, from 0.4- to 0.6 cm. (from about \ to i in.). 

Generally speaking, the size of the heart corresponds to the size and 
the development of the individual. In judging of an increase or decrease 
in its size, we must consider the weight of the organ and the thickness 



POST-MORTEM EXAMINATIONS. 23 

of its walls. If the person die while the heart is contracted, the walls 
of the ventricles will appear thicker, their cavities smaller than usual. 
If he die of some exhausting disease, like typhoid fever, or if decompo- 
sition have commenced, the heart-walls will usually be flabby and the 
cavities will appear larger than usual. 

Preservation of Specimens. — Parenchymatous and fatty degeneration of the heart- 
muscle are best studied microscopically by teasing the fresh muscle in one-half -per- 
cent salt solution, or by examining in the same solution fresh sections made with the 
freezing microtome. For the study of interstitial changes, fatty infiltration, etc., small 
pieces of the heart-muscle should be hardened in Miiller's fluid. The valves may be 
stretched on a flat cork with pins, laid for forty-eight hours in a mixture of equal parts 
of one-sixth-per-cent chromic acid and alcohol, and then transferred to strong alcohol. 
For the methods of detecting bacteria in ulcerative endocarditis, see section on Bac- 
teria Staining. When the presence of bacteria is suspected, the specimen should be 
preserved in strong alcohol. 

The Pleural Cavities are next examined. The hand is passed into 
each, and the existence of serous or fibrinous exudations or of old adhe- 
sions ascertained. The method of detecting the presence of air has been 
given above. After the commencement of putrefaction, reddish serum 
may accumulate in the pleural cavities. This should not be mistaken 
for the result of disease. 

The Lungs. — Each lung is lifted up in turn, the vessels, etc., at its 
base divided, and the organ removed. If the pleura is very adherent, it 
is better to strip off the costal pleura with the lung. After inspecting 
the external surface of the lung, observing its size, shape, color, and 
consistency, we open the bronchi. For this purpose we use scissors with 
long, narrow, blunt-pointed blades, one blade a little longer than the 
other. The lung is held in the left hand with its base upward. We 
first open the large bronchi which run on the inner side of the lower 
lobe, afterward those of the upper lobe. Each bronchus should be fol- 
lowed to its smaller ramifications. 

We should observe the contents of the bronchi and the appearance of 
their walls. In the larger and medium-size bronchi, the cartilages in 
their walls do not form complete rings, but appear shining through the 
mucous membrane like irregular white patches. This appearance should 
not be mistaken for a pathological change. In bodies which have been 
dead for some time, especially in cold weather, the bronchial mucous 
membrane may be red and swollen as a post-mortem change. The contents 
of the stomach are sometimes forced, after death, into the pharynx, and 
thence find their way into the trachea and bronchi, giving them a pe- 
culiar reddish and even gangrenous appearance. Bronchitis does not 
always leave lesions which can be seen after death. 

After the examination of the bronchi, the lung is turned over, the 
vessels, etc., at its root grasped with the left hand, and a long, deep 



24 THE METHOD OF MAKING 

incision made from apex to base. We observe the appearance and texture 
of the lungs, whether the air vesicles are dilated (ernplrysematous) or 
filled with serum, blood, or inflammatory exudation. Fluid can be 
pressed out of the air vesicles without breaking down the lung tissue. 
Solid inflammatory exudation, on the other hand, renders the lung more 
resistant and easily broken down. Attention should be paid to the oozing 
of purulent or other fluid from the smaller bronchi when the lung is 
squeezed near the cut surface. It is the rule to find the lower lobes more 
congested than the upper. 

Preservation of the Lungs and Bronchi. — If the lungs have been cut, small pieces 
from the affected portions of lung tissue or bronchi should be hardened in Miiller's 
fluid, care being taken not to squeeze or handle them unnecessarily. It is better, when 
the microscopical examination is more important than the macroscopical, not to open 
the lungs at once, but to till the air spaces with preservative fluid by means of a funnel 
attached to a short rubber tube and canula, which is tied into the main bronchus. In 
this way, not only are the minute structures preserved better, but the air vesicles are 
filled out and hardened in an approximately natural condition. Care should be taken 
not to have too great a pressure from the inflowing fluid, since then exudations might 
be displaced or the lung distorted or ruptured. While the lung is being filled, it 
should be immersed in a vessel of the same preservative fluid, in which it lies for 
twenty-four hours. It is then cut into small pieces, and the hardening completed. A 
variety of hardening agents may be used : Miiller's fluid, strong alcohol, or the mix- 
ture of equal parts of one-sixth-per-cent solution of chromic acid and alcohol. For 
general purposes the latter fluid is perhaps the best. If, however, the lung is com- 
mencing to decay, strong alcohol will stop the process more quickly, and give as good 
results as are possible under the circumstances. Alcohol should be used when the 
lungs are to be examined for bacteria. 

It is often desirable, and particularly in cases in which the topography of lesions is 
to be studied, as in acute miliary tuberculosis, acute and chronic phthisis, infarctions, 
etc., to inject the blood-vessels with colored gelatin. The lung should, after the injec- 
tion, be hardened in alcohol. 

The Pharynx, Larynx, (Esophagus, and Thyroid Gland. — For the 
removal of these parts, the incision through the skin should be carried 
upward as far as practicable — when allowable, to a point one inch below 
the chin, the head being allowed to hang backward over the edge of the 
table. 

The soft parts are dissected from the larynx, taking care not to cut 
the thyroid body, and an incision is made through the floor of the mouth, 
following the internal surface of the inferior maxilla. Through this 
incision the fingers are introduced into the mouth, the tongue drawn 
down, the posterior wall of the pharynx divided above the tonsils, and 
the pharynx and larynx drawn out together. These organs are then 
pulled downward, and with the aid of the knife the trachea and oeso- 
phagus are removed entire, the oesophagus being cut just above the 
stomach. If the contents of the stomach are to be preserved, as in cases 
of suspected poisoning, a ligature is put around the oesophagus just below 
the point at which it is to be cut off. 



POST-MORTEM EXAMINATIONS. 25 

With the enterotome the pharynx and oesophagus are now slit open 
upon their posterior surfaces. The mucous membrane thus exposed is 
examined for evidences of caustic poisons, of inflammation, tumors, stric- 
tures, etc. The enterotome is next introduced into the larynx, and this 
organ and the trachea laid open along the posterior wall. Here we look 
for cedema of the aryteno-epiglottidean folds (cedema of the glottis), for 
evidences of catarrhal, croupous, ulcerative, and syphilitic inflammation, 
and for tumors and lesions of the laryngeal cartilages. (Edema and red- 
ness of the larynx may be produced by post-mortem changes, especially 
in bodies which have been kept for several days in cold weather. A well- 
marked cedema glottidis during life may leave no trace after death. 
Putrefactive changes usually commence early in the larynx and trachea. 

The thyroid gland is dissected off and examined. Its weight varies 
a good deal, being, according to Krause, somewhat over 30 gm. 
(about 1-J oz.). 

Preservation of the Larynx, Trachea, etc. — The larynx and trachea are freed from 
superfluous tissue and suspended entire by a thread in a large quantity of a mixture 
of equal parts of one-sixth-per-cent chromic acid and alcohol. The mixture should 
be renewed at the end of twenty-four hours, and again on the third and sixth days; at 
the end of ten days the specimen is washed and transferred to strong alcohol, in 
which it is preserved. The oesophagus should be stretched on a flat cork with pins, 
and then treated in the same way. For bacterial study the specimens should be pre- 
served in alcohol. The thyroid may be cut into small pieces, and hardened either in 
Muller's fluid or alcohol. 

THE ABDOMEN. 

Eeturning now to the abdominal cavity, we first dissect off the omen- 
tum. If tubercles of the peritoneum exist, they are best seen and 
studied in the omentum. The colon is then raised and dissected free, 
to the cascum on one side and to the rectum on the other. The colon 
and small intestines are then drawn first to the right and then to the 
left side, so as to expose in turn the right and left kidneys. As each 
kidney is brought into view, an incision is made through the peritoneum 
over the track of the ureter. The ureter is followed through its entire 
length and its condition ascertained. 

The Kidneys are then removed, separating the peritoneum and fat 
from them with the hand, and dividing the vessels with the knife. The 
suprarenal capsules, which are attached to the upper end of each kidney, 
are removed at the same time. The kidneys may be softened by putre- 
faction, or the surface may have a greenish-gray color, caused by the 
post-mortem action of putrefactive gases on the hemoglobin. 

An incision is made through the capsule, along the convex border of 
the kidney, and the membrane stripped off. We notice the degree of 
adherence of the capsule to the kidney, and also the surface of the latter, 
whether smooth or roughened, pale, congested, or mottled; an incision 



26 THE METHOD OF MAKING 

is made along the convex surface down to the pelvis, so that the organ 
is divided into halves. We observe the relative thickness of the cortical 
and pyramidal portions, as well as the size of the entire organ. To as- 
certain the latter point, it is well to weigh each kidney; the normal 
weight is from 130 to 150 gm. (about 4J to 5 oz.). 

It is necessary to remember, however, that in a kidney which is 
much atrophied there may be an increase of fat in the pelvis, which 
gives the organ nearly its normal size and weight, while the kidney 
tissue proper may have in great measure disappeared. 

The weight of the kidneys of adults is given by Vierordt in general 
as about 0.48$ of that of the entire body. 

We now inspect the kidney tissue more closely, especially the cortical 
portion. The pyramids consist largely of tubes running in nearly 
straight lines from the apex to the base of each pyramid. These straight 
tubes pass from the pyramids into the cortex in bundles, called medul- 
lary rays, many of them retaining their straight course until they nearly 
reach the surface of the kidney. These straight tubules send off branches 
on all sides of the rays, which become convoluted, form Henle's loops, 
and finally terminate in the glomeruli or Malpighian bodies. In this 
way the cortex of the kidney, as seen in section, is divided into alternate 
bands of straight tubes, convoluted tubes and glomeruli; both sets of 
bands being perpendicular to the surface of the kidney, and called re- 
spectively medullary rays and labyrinths. About the convoluted tubules 
and glomeruli is a rich venous plexus; and since after death the blood 
usually remains in this plexus and in the glomeruli, the bands contain- 
ing the convoluted tubules, i.e., the labyrinths, usually appear red, 
while the medullary rays are grayish-white. In a normal kidney, there- 
fore, the cortex should be regularly striped in narrow alternating red 
and whitish bands. 

The average thickness of the cortex of the kidney is about one-third 
of an inch. 

If there be extensive congestion, the entire cortex is red. If the epi- 
thelium of the tubules degenerates and fills thetn up, or if there are 
considerable changes in the interstitial tissue, the regular bands are lost 
and the cortex is irregularly mottled. If the tubular epithelium be- 
comes filled with fat-globules, this is indicated by an opaque yellow color 
of the affected parts; in many cases, therefore, the existence of kidney 
disease can be recognized with the naked eye. 

If waxy degeneration be present to a marked extent, it may be mani- 
fest by a peculiar translucent appearance of the affected parts, but in 
most cases it is necessary to apply reagents to demonstrate it satisfac- 
torily. The cut surface of the kidney is washed with water to free it 
from blood, and repeatedly brushed with an aqueous solution of iodine 
(iodine 1 part, potassium iodide 3 parts, water 100 parts). The glome- 



POST-MORTEM EXAMINATIONS 27 

ruli and the blood-vessels are most frequently affected, and, if so, they 
will appear as mahogany-colored dots and lines on a yellow ground. 

The pelvis should be examined for inflammatory lesions and calculi. 
Sometimes a whitish fluid is seen in the pelvis, and can be squeezed from 
the papillae; this is produced by a post-mortem desquamation of the 
epithelium, but is liable to be mistaken for pus. 

Preservation of the Kidney. — If the kidney be not opened, the blood-vessels may be 
injected through the renal artery with alcohol; or, which is better, after washing out 
the blood-vessels with one-fifth-per-cent solution of chromic acid, the organ may be 
injected slowly under a low pressure with " Delafidd's osmic acid mixture " (see p. 44). 

After filling the kidney well with this solution, the vessels are tied and the entire 
organs placed in eighty-per-cent alcohol for twenty-four hours. It is then cut into 
small pieces and preserved in eighty-per-cent alcohol. 

Instead of injecting the organ, small pieces may be cut out and hardened in the 
osmic acid mixture. This in most cases will be the routine practice, as the osmic 
acid is expensive and the operation of injection somewhat troublesome. 

Kidneys which are to be examined for the presence of bacteria should be cut into 
small pieces and placed at once in strong alcohol, which should be changed once or 
twice, and in which they are permanently preserved. 

The Suprarenal Capsules are in the foetus of an ovoidal, in the adult 
of a triangular shape. They are situated at the upper and inner border 
of the kidney, to which they are loosely attached by connective tissue. 
On the anterior surface is an irregular fissure, called the hilus, from 
which the veins emerge. The size varies considerably, but in the adult 
the average vertical diameter is from 3.2 cm. (1^ in.) to 4.5 cm. (If in.); 
the transverse diameter about 3.2 cm. (l^ in.), and they are from 4.2 
mm. (^ in.) to 6.4 mm. (-J in.) in thickness. They weigh in the adult 
from about 4 gm. (1 3 ) to 8 gm. (2 3 ). They are composed of a cor- 
tical and medullary portion, the cortex forming a yellowish shell around 
the dark-red or brown medulla. They are inclosed in a connective-tis- 
sue capsule, from which fibrous processes extend inward, dividing the 
gland into a series of irregular chambers. Those in the cortex are 
mostly elongated, giving this portion a striated appearance, while those 
in the medulla are polyhedral. It is in these spaces that the parenchyma 
cells lie. The suprarenal capsules readily decompose ; the inner layer of 
the cortex may soften and break down, so that the outer zone forms a 
sort of cyst filled with reddish-brown broken-down substance. Hyper- 
trophy, tuberculosis and cheesy degeneration, fatty degeneration, and 
tumors are to be looked for. 

Preservation. — The suprarenal capsules should be hardened in Muller's fluid or in 
strong alcohol. 

The Spleen. — This organ has, when removed from the body, the gene- 
ral shape of a flattened ellipsoid, most curved on its external and posterior 
surface. It is situated in an oblique position on the left side of the stom- 
ach, and between its cardiac end and the diaphragm. The vessels are 



28 THE METHOD OF MAKING 

given off from its inner surface, which is crossed by a more or less well- 
marked vertical ridge. The point of emergence of the vessels is called 
the hilus. Its long diameter extends from the seventh intercostal space 
to the eleventh rib. Its upper portion is separated from the ribs by the 
lungs ; its lower portion by the diaphragm. 

Its usual length in the adult is, according to Vierordt, from 1Z to 13 
cm. (about 4f to 5 in.); its breadth from 7 to 8 cm. (about 2f to 3 
in.); its thickness 3 cm. (about 1^ in.). Its average weight is about 
171 gm. (about 7 oz ). The dimensions of the spleen as given by Krause 
are somewhat greater than the above. But its measurement and weight 
vary considerably within the limits of health. It is in these respects the 
most variable organ in the body. In old age the average weight gradu- 
ally diminishes. 

The spleen is inclosed in a fibrous capsule covered with peritoneum. 
The parenchyma is formed of blood-vessels and fibrillar connective tissue, 
and of a soft, dark-red pulp in which are imbedded whitish spheroidal 
or elongated bodies, the glomeruli or Malpighian bodies. In the normal 
human spleen the glomeruli are hardly perceptible to the naked eye, but 
sometimes they are very plain. Sometimes the fibrous stroma is very 
apparent ; sometimes not. 

The size, consistence, and color of the organ vary a good deal with- 
out any known cause. Decomposition softens it. Thickenings of the 
capsule and abnormal adhesions are very common, and often occur with- 
out any clinical history indicating disease. We should look for changes 
in size, pigmentations, hyperplasia of the connective tissue, amyloid de- 
generation, tubercles, and infarctions. 

Not infrequently one or more spheroidal or flattened so-called acces- 
sory spleens are found in the vicinity of the spleen ; they vary in size 
from that of a pea to that of a walnut. 

Preservation. — In certain diseases of the pulp, leukaemia, leucocythaemia, etc., the 
tissue should be teased, when fresh, in one-half-per-cent salt solution. For general 
purposes, small pieces of the organ are hardened in Muller's fluid. 

The Intestines. — The rectum is divided, the intestine seized with the 
left hand, and, being kept stretched, is separated from its attachments 
by repeated incisions through the mesentery close to the gut, until the 
duodenum is reached, where it is again cut off. The operation is more 
cleanly if, before dividing the gut, ligatures are placed around it at either 
end. The entire length of the gut is now laid open with the enterotome 
along the mesenteric attachment, the mucous membrane is cleaned with 
a stream of water and then examined. 

In cases of suspected poisoning, a ligature should be placed around 
the rectal end of the gut and two around the duodenal end, and it is then 
cut off below the former and between the latter ligatures. The gut is 



POST-MORTEM EXAMINATIONS. 29 

now opened, and the contents emptied into a clean glass jar for delivery 
to the chemist, care being taken that they be not allowed to touch any- 
thing but the inner surface of the jar. After washing the intestine in 
pure fresh water and examining it, it should be placed entire in another 
clean jar and sealed. 

Cadaveric lividities are very common in the intestines, and are usu- 
ally most marked in the dependent portions. They are apt to occur in 
patches, but may be diffuse and very extensive. If the wall of the gut 
be stretched, they are often seen to be discontinuous, owing to the pres- 
sure of the blood from the parts which are squeezed by folds. Small 
patches of arborescent or diffuse red staining are often seen, formed by 
the imbibition from the vessels of decomposing haemoglobin. In the 
more advanced stages of decomposition, the mucosa may be softened 
and loosened. A dark purple or brownish discoloration of the entire 
intestinal wall is frequently seen, either diffuse or in patches. Much 
experience and careful observation are requisite in forming a correct 
judgment regarding the significance of changes of color in the intestines. 
Caution is necessary in distinguishing normal digestive hyperemia from 
abnormal congestion. A very considerable congestion may exist without 
disease. In cholera seasons especially, observers are prone to call the 
most moderate degree of congestion abnormal. 

The lesions ordinarily to be looked for are catarrhal, croupous, and 
ulcerative inflammations, perforations, haemorrhages, strictures, tumors, 
amyloid degeneration, swelling and ulceration of the solitary follicles 
and Peyer's patches, and pigmentation. For the detection of amyloid 
degeneration of the mucosa, this structure should be carefully washed 
and brushed with a solution of iodine (see p. 26). 

Preservation. — For the general purposes of microscopic study, portions of the gut 
should be gently stretched on cork (the mucosa side free) and placed for a few minutes 
in strong alcohol, and then transferred to eighty-per-cent alcohol, in which the hardening 
is completed. The transfer to weaker alcohol is to prevent the specimen from becom- 
ing brittle. 

For obvious reasons, the mucous membrane should be handled as little as possible, 
for, in the majority of cases, decomposition and softening have already set in at the 
time of the autopsy, and, under the most favorable conditions, the epithelium is very 
easily rubbed off. 

The Stomach and Duodenum. — We now introduce the enterotome into 
the duodenum, at its transverse portion, and open it on the convex 
border. When the pylorus is reached, the incision is carried obliquely 
over to the greater curvature of the stomach, along which it is extended 
as far as the oesophageal opening, and the organ examined in situ; or, if 
a more careful examination of the stomach is called for, after ascertain- 
ing whether or not the bile-duct is pervious (see below), the duodenum 
and stomach may be removed together, and the stomach opened and 



30 THE METHOD OF MAKING 

examined on the table. (If poisoning be suspected, a ligature should 
have been placed earlier in the examination, see above, around the lower 
end of the oesophagus and the duodenum. The stomach and duodenum 
are now removed together unopened. They are to be opened in a care- 
fully cleansed glass jar, and after an inspection of the mucous membrane 
and the contents witli the naked eye and a hand-lens, stomach, duo- 
denum, and contents are to be sealed in the jar for the chemist.) 

We now look for the orifice of the bile-duct, which will be found 
about the middle or the descending portion of the duodenum on its con- 
cave border. Pressure on the gall-bladder or on the common duct will 
cause the bile to flow into the intestine if the ducts are pervious. But a. 
sufficient degree of stoppage may exist in the ducts to give rise to marked 
symptoms of disease without preventing the flow of bile under these con- 
ditions, even with a moderate pressure. A long director is now passed 
into the gall-duct, which is laid completely open ; ulcerations, cicatrices, 
gall-stones, inflammatory lesions, and tumors are looked for. In stricture 
of the gall-duct, the mucous membrane above will often be found bile- 
stained, while below it is colorless. At this point, should there be any 
special reason for doing so, the portal vein, which lies close behind the 
ductus choledochus, should be opened and examined for periphlebitis, 
phlebitis, and thrombosis. The mucous membrane of the duodenum 
and stomach are now rinsed off and examined. Acute inflammations 
from caustic poisons, chronic catarrhal inflammations, haemorrhages, 
ulcers, erosions, swelling of the solitary follicles, and tumors are lesions 
most frequently seen. We sometimes find a diffuse congestion of the 
stomach similar to that produced by irritant poisons, as a result of doses 
of croton oil given just before death. 

Preservation. — The same methods should be used as for the intestines (see above). 
Tumors should be cut into small pieces and hardened in Mutter's fluid. 

The Liver. — To remove the liver, the diaphragm is first divided on 
one side of the suspensory ligament as far back as the spine; the suspen- 
sory ligament is then divided; then the right and left lobes being in turn 
raised, the lateral ligaments are severed. Then, seizing the left lobe, the 
organ is dragged obliquely downward into the abdominal cavity, the re- 
maining attachments being dissected away. The liver is first laid on its. 
superior surface, and the gall-bladder and its contents examined. The 
character of the gall is to be determined, and gall-stones, inflammatory 
lesions, and tumors sought for. To determine the actual size of the 
organ, it should be both measured and weighed. Its size varies greatly 
in different healthy individuals, but in general it may be said that it 
measures from 25' to 30 cm. (10 to 12 in.) transversely; from 15.3 to 18 
cm. (6 to 7 in.) antero-posteriorly, and about 9 cm. (3£ in.) at its 
thickest part; the ordinary bulk is about 229 to 252 c.c. (90 to 100 cu.. 
in.); its ordinary weight between 1,550 to 1,860 gm. (50 to GO oz.).. 



POST-MORTEM EXAMINATIONS. 31 

In children, its weight relative to that of the body is greater than in 
adnlts. The liver is increased in size and weight during digestion and 
by congestion from any cause. 

The surface of the liver is now examined, and it is then laid on its 
lower surface and several deep incisions made from the convex surface 
downward. The color and consistence of the liver tissue should be 
noticed, also the distinctness with which the lobular outlines can be 
seen; whether or not the centres of the lobules are congested or their 
peripheries lighter in color than usual; the presence of tumors, tuber- 
cles, abscess, ecchinococcus, new connective tissue, and pigmentation. 
Suspected amyloid degeneration should be tested for by the iodine solu- 
tion (p. 26). 

We often find the surface of the liver of a greenish or very dark- 
brown color; less frequently the same color extends into the substance 
of the organ. This discoloration, which is entirely post-mortem, is, like 
the similar discoloration of other internal organs, produced by the action 
of the gases or putrefaction on the coloring matter of the blood. 

Preservation. — For the study of parenchymatous degeneration, sections of the 
fresh frozen tissue or small teased fragments should be examined in half-per-cent salt 
solution. For general purposes, small pieces should be hardened in Miiller's fluid. 
Tumors should be treated in the same way. In many cases of marked cirrhosis, the 
topography of the lesion is best demonstrated by injecting the organ with blue gelatin 
through the portal vein and then hardening in strong alcohol. 

The Pancreas. — This organ, of a light yellowish-red color, is elon- 
gated, irregularly prismatic in shape, and flattened antero posteriorly; 
the right end, called the head, is broader than the rest, and lies in the 
concavity of the duodenum. The remainder of the organ, the body and 
tail, are usually tapering, and lie transversely in the abdominal cavity, 
the tail reaching to the spleen. Its size and weight vary considerably; 
its usual length is from 15.3 to 20.3 cm. (6 to 8 in.); its breadth about 
3.8 cm. (l-g-in.); its thickness about 1.3 to 2.5 cm. (J to 1 in.); its 
weight is usually from 70 to 108 gm. (2J to 3£ oz.) The organ may be 
rounded instead of flattened; the head and tail may be disproportion- 
ately large; the tail may be unusually long or may be divided or curved. 
The superior mesenteric artery and vein which pass behind the gland 
are usually partly imbedded in it, but are sometimes completely in- 
closed. 

A longitudinal incision should be made through the whole gland, 
which may remain in situ, and its substance and duct should be searched 
for calculi, tumors, malformations, and evidences of acute and chronic 
inflammation and amyloid degeneration of the blood-vessels. The pan- 
creas is frequently of a dark-red color from post-mortem staining. 

Preservation. — Portions of this organ should be hardened in strong alcohol, and 
not in chromic salts, which destroy the gland cells. 



32 THE METHOD OF MAKING 



THE GENTTO-TJRINARY ORGANS. 



The Male Organs. — If the urine is to be examined, it may be drawn 
off with a catheter; or a vertical incision may be made into the bladder, 
just above the symphysis pubis, and some of the urine dipped out. The 
cut end of the rectum should now be grasped with the left hand and 
raised up, and this and the bladder, prostate gland, etc., dissected away 
from the pelvis, the knife being carried close to the bone. The bladder 
is now drawn backward, and the loose tissue close under the symphysis 
pubis cut. The body of the penis is then shoved backward within the 
skin and dissected away from behind beneath the symphysis, and finally 
cut off just behind the glans penis. The penis and bladder are now 
drawn backward and upward, and the pelvic organs removed together. 
Or the penis may be removed by sawing away the bones above the pubic 
arch, and then dissecting away the penis, whose root is thus exposed. 

The pelvic organs are then laid on the table, the bladder uppermost; 
a long director is passed into the urethra, which is opened on its upper 
surface through its entire length and the bladder widely opened. In 
the urethra, the presence of strictures, diverticular, ulcers, inflammatory 
lesions is to be noticed; in the bladder, inflammatory lesions, hypertro- 
phies, congestion, and ecchymosis of the mucous membrane and tumors. 
The organs are now turned over; the rectum opened and examined for 
varicose veins, haemorrhages, ulcers, strictures, and tumors. The pros- 
tate gland is then cut into and the presence of calculi, inflammatory 
lesions, hypertrophies, and tumors sought for. Lastly, the vesicular 
seminales are examined, in which, though rarely, we may find evidences 
of tubercular inflammation and dilatation. 

The Testicles- may be removed, when necessary, without cutting the 
scrotum, by enlarging the inguinal canals from within, and crowding 
the glands through them and cutting them off. The average weight of 
the adult testicle with its epididymis is, according to Krause, from 15 
to 24.5 gm. (about from J to f oz.). Inflammatory lesions, tubercu- 
losis, abscesses, and tumors are the most frequent lesions. 

Preservation. — The urethral canal and bladder may be pinned open and hardened 
in alcohol. The prostate, vesiculse seminales, testicles, and tumors should be hard- 
ened in Muller's fluid or alcohol. 

The Female Organs. — The position and general condition of the pel- 
vic organs should first be determined by inspection. Abnormal adhe- 
sions of the ovaries, broad ligament, Fallopian tubes, and uterus; malpo- 
sitions of the uterus; subserous tumors of the uterus and ovarian tumors, 
are frequently observed. Haemorrhage into the posterior cul-de-sac is 
sometimes found. The urine should be collected, if necessary, as above 
directed; the organs should be dissected away laterally, as in the male, 



POST-MORTEM EXAMINATIONS. 33 

care being taken not to injure the ovaries and Fallopian tubes. The 
bladder is then drawn strongly backward and upward, and dissected 
away from the symphysis and the pubic arch, and, the point of the knife 
being carried forward and downward, the vagina is cut off in its lower 
third, the rectum severed just above the anus, the remaining attachments 
cut, and the pelvic organs taken out together. If it be necessary to 
remove the external generative organs, after freeing the lateral surfaces 
of the internal organs and the bladder, the legs are widely separated and 
the vulva and anus circumscribed by a deep incision. The tissues close 
beneath the pubic arch are now dissected away from below and the vulva 
thrust back beneath the symphysis; it is now seized above the bone, and 
together with the anus dissected away and removed with the other 
organs. 

The Bladder is first opened and examined. The vulva may now be 
examined for hypertrophies, inflammatory lesions, ulcers, cicatrices, 
cysts, and tumors. The Vagina is opened along the anterior surface; its 
more common lesions are inflammations, fistula?, ulcers, tumors, and 
rarely cysts. 

The Uterus, — Before opening this organ, its size and shape should be 
determined. The adult virgin uterus is a pear-shaped body, flattened 
antero-posteriorly; the upper portion, or body, is directed upward and 
forward, whilst the lower portion, the cervix, is directed downward and 
backward. It is covered anteriorly by peritoneum to a point a little 
below the level of the os internum; posteriorly, to a point a little below 
the level of its junction with the vagina. The peritoneal investment 
separates from the organ at the sides to form the broad ligaments. The 
uterus is held in position by the broad and round ligaments and by its 
attachments to the bladder and rectum and vagina. The upper end, 
the fundus, does not extend above the level of the brim of the pelvis. 
Its average length is about 7.6 cm. (3 in.); its breadth about 5.1 cm. 
(2 in.); its thickness about 2.5 cm. (1 in.); its average weight is about 
31 to 46 gm. (1 to 1^ oz.). During menstruation the uterus is slightly 
enlarged, and the mucous membrane of the body becomes thicker, softer, 
and its vessels engorged with blood; while its inner surface is more or 
less thickly covered with blood and cell detritus. A description of the 
complicated changes in the uterus which pregnancy entails may be found 
in the works on obstetrics. After pregnancy, the uterus does not return 
to its original size, but remains somewhat larger; the os is wider and 
frequently fissured. 

We not infrequently find in the mucous membrane of the lower part 
of the cervix, small transparent, spheroidal structures called ovula 
Nabothi; these are small retention cysts caused by the closure of the 
orifices of the mucous glands of the part. The more common lesions 
observed in the uterus are malpositions, malformations, lacerations, ulcera- 
3 



34 THE METHOD OF MAKING 

tions of the cervix, acute and chronic inflammation of the mucous mem- 
brane or muscularis, or both, thrombosis and inflammation of the veins 
and tumors. 

In the infant the uterus is small, the body flattened, the cervix dis- 
proportionately large. During childhood the organ increases in size, 
but the body remains small in proportion to the cervix. At puberty the 
shape changes and the body becomes larger. 

The Ovaries are flattened, ovoidal bodies, situated one on each side 
and lying nearly horizontally at the back of the broad ligament of the 
uterus. Their size is variable and they are usually largest in the virgin 
state. Their average weight is from 3.9 to 6.5 gm. (3 to 5 3). They 
measure about 3.8 cm. (1| in.) in length, 1.9 cm. (f in.) in breadth, and 
nearly 1.3 cm. (^ in.) in thickness. The sides of the ovary and its pos- 
terior border are free; it is attached along the anterior border; to its end 
is attached the ovarian ligament; to its outer extremity one of the fim- 
briae of the Fallopian tube. The ovary is covered on its free surface by 
cylindrical epithelium, and its surface is less glistening than the general 
peritoneum. The surface of the ovary is smooth in the young, but be- 
comes rougher and depressed in spots as the process of ovulation goes on. 
In adult females we usually find corpora lutea in their various stages. 
We should seek for evidences of acute and chronic inflammations, for 
tumors and cysts. 

The Fallopian Tubes, lying in the upper margin of the broad liga- 
ments, are from 7.6 to 10 cm. (3 to 4 in.) in length. The length 
often differs considerably on the two sides. They commence at the upper 
angles of the uterus as small perforated cords, which become larger fur- 
ther outward, and bend backward and downward towards the ovary. They 
terminate in an expanded fimbriated extremity about 2.5 cm. (1 in.) 
beyond the ovary. They are covered by peritoneum, and the mucous 
membrane lining them, continuous with that of the uterus, is thrown 
into longitudinal folds. Malpositions by adhesions, closure, inflamma- 
tions, and cysts are the more common lesions. The possibility of tubal 
pregnancy should be borne in mind. 

Preservation. — All of these organs and their tumors may be hardened in Muller's 
fluid or in alcohol. The vagina should be stretched flat on cork and the cavity of the 
uterus laid wide open. Great care should be taken not to touch either the internal 
surface of the uterus or the external surfaces of the ovaries, since in both the epithe- 
lium is very easily rubbed off. 

It is better, after opening them by a transverse incision, to suspend the ovaries by 
a thread in a jar of the preservative fluid than to let them lie on the bottom, since the 
epithelium is thus less liable to be rubbed off. ' 

1 Absolute and relative sizes and weights of various parts and organs of the body, 
and much other valuable statistical data, may be found in VierordVs " Anatomische, 
Physiologische und Physikalische Daten und Tabellen," Jena, 1888. 



POST-MORTEM EXAMINATIONS. 35 

AUTOPSIES IN CASES OF SUSPECTED POISONING. 

It is always best, in cases of suspected poisoning, to preserve for the 
chemist not only the stomach and intestine, but the entire liver and brain; 
or if portions of these only can be saved, these portions should be carefully 
weighed, as well as the entire organs, and the relative amount of tissue 
reserved carefully noted at the time It is even well, particularly in 
cases in which the administration of the readily diffusible poisons, such 
as arsenic, strychnia, etc., is suspected, to preserve the whole of all of 
the internal organs, together with a large piece of muscle and bone; since 
with large quantities of tissue the results of the chemical analysis depend 
less upon calculations, and are hence more comprehensible to the average 
jury. In all such- cases, jars should, if possible, be procured which have 
never been used before, and these should be carefully washed and rinsed 
with distilled water. They should have glass stoppers and be sealed at 
once and carefully labelled before leaving the hands of the operator. If 
they can be delivered to the chemist without much delay, they should 
have no preservative fluid added. If they are to be kept for a consider- 
able time, pending the action of a coroner's jury or for some other rea- 
son, a small quantity of pure, strong alcohol may be poured over them. 
In this case, the operator should be particular to reserve a quantity, at 
least half a pint, of the specimen of alcohol used, in a clean sealed and 
labelled bottle, so that this may be tested by the chemist and be proven 
to be free from the poison. It is better in all cases, however, to avoid, 
if possible, the use of alcohol. In all autopsies which may have medico- 
legal importance, fu'1 notes should be taken by an assistant as the opera- 
tion proceeds, carefully read over immediately afterwards, and dated and 
kept by the operator for future reference. The labelling and disposition 
of the jars should be recorded in the notes. 



EXAMINATION OF THE BODIES OF NEW- 
BORN CHILDREN. 

In examining the bodies of new-born children, we may have to deter- 
mine, besides the ordinary lesions of disease, the age of the child, 
whether it was born alive, how long it has been dead, what was the 
cause of death. 

GENERAL INSPECTION. 

The Size and Age. — Caspar 1 gives the following description of the 
foetus during the different months of intra-uterine life. 

1 Caspar, " Handbook of Forensic Medicine.' Revised German Edition by Li man, 
1882, p. 865 et seq. ; or Sydenham Society Translation. 



36 THE METHOD OF MAKING 

At the fourth week, the embryo is 8 to 13 mm. (^ to T 5 F in.) long. 
The cleft of the mouth and two points indicating the eyes can be recog- 
nized in the head. The extremities are represented by little wart-like 
projections. The heart can be distinguished,, the liver is disproportion- 
ately large. The umbilical vessels are not yet formed. The entire 
ovum has about the size of a walnut. 

At the eighth tueek, the embryo is 2.3 to 4 cm. ( T 9 F to 1^ in.) long. 
The head forms more than a third of the entire body; the mouth is very 
large; the nose and lips can be distinguished, but not the external ear. 
The hand is longer than the forearm; the fingers are formed, but joined 
together; the toes look like little buds; the soles of the feet are turned 
inward. The position of the anus is indicated by a point. The abdo- 
men is closed. All the viscera can be recognized. Centres of ossifica- 
tion are formed in the apophysis of the first cervical vertebra, the 
humerus, radius, scapula, ribs, and cranial bones. There are rudimen- 
tary external genitals, but the sex can hardly be distinguished. The 
ovum has about the size of a hen's egg. 

At the twelfth week, the placenta is formed. The embryo is 5 to 6.5 
cm. (2 to 2-J-in.) long, and weighs about 31 gm. The head is sep- 
arated from the thorax by a distinct neck. The eyes and mouth are 
closed. The nails can be perceived on the fingers. The sex can be 
recognized. The umbilical cord is inserted near the pubes; the muscles 
begin to be recognizable. The thymus and suprarenal capsules are 
formed. The cerebrum, cerebellum, medulla, and the cavities of the 
heart can be recognized. The humerus is 1.7 mm. long; the radius 5.5 
mm.; the ulna 6.6 mm.; the femur and tibia 4.4 to 6.6 mm.; the fibula 
5.5 mm. The ovum is as large as a goose's egg. 

At the sixteenth week, the embryo is 13 to 15 cm. (5 to 6 in.) long, 
and weighs 77 to 93 gm. (2J to 3 oz.). The skin is of a rose-red color 
and has considerable consistency. The formation of fat in the subcuta- 
neous tissue has begun. The scrotum and labia are formed. The face 
begins to assume its characteristic appearance. There is whitish meco- 
nium in the duodenum. The liver is not so disproportionately large, 
and the gall-bladder is formed; the anus is open. The length of the 
humerus, radius, and ulna is 1.7 cm.; the femur and tibia 8.8 toll 
cm. The calcaneus begins to ossify at the middle of the fourth month. 

At the ttventieth iveek, the embryo is 26 to 28 cm. (10 to 11 in.) 
long; it weighs from 225 to 320 gm. (7 T 3 F to 10 oz.). The nails are 
quite perceptible. There is a thin down on the head. The head is 
still disproportionately large, occupying about one-fourth of the body. 
There is as yet none of the vernix caseosa. The secretion of bile has 
commenced and stains the meconium. The insertion of the umbilical 
cord is still further off from the pubes. The liver, heart, and kidneys 
are large in proportion to the other organs. The convolutions of the 



POST-MORTEM EXAMINATIONS. 37 

brain cannot be recognized. The humerus is 2.8 to 3 cm. long; the 
radius 2.6 cm.; the ulna 2.8 cm.; the femur, tibia, and tibula, each 2.6 
cm. The astragalus and the upper part of the sternum begin to 
ossify. 

From this time on, the length of the foetus forms an approximately 
accurate basis for the estimation of its age. From this period till its 
maturity, the length of the foetus, determined in centimetres, corresponds 
to about one-fifth of the number of months of its age. From this time 
on, the weight exhibits marked individual differences, and is therefore 
a less reliable criterion of its age than is the length. 

At the twenty-fourth tveek, the embryo is 31 to 34 cm. (12 to 13 in.) 
long, and weighs 750 to 875 gm. (24 to 28 oz.). The lanugo and ver- 
nix caseosa are formed. The skin is of a dusky cinnabar-red color. 
The meconium is darker. The scrotum is empty, small, and red; the 
labia majora are prominent and held apart by the projecting clitoris. 
The pupillary membrane is present and readily recognized. The length 
of the humerus and radius is 3.5 cm.; of the ulna, femur, tibia, and 
fibula, each 3.7 cm. 

At the twenty-eighth week, the embryo is 36.4 to 39 cm. (14J- to 15J 
in.) long, and weighs 1,500 to 1,750 gm. (48 to 57 oz.). The hair is 
more abundant and longer. The great fontanelle measures about 4 cm. 
(If in.) in diameter, and all of the fontanelles are readily perceived. 
The skin is of a dirty reddish color and abundantly beset with the lanugo 
and vernix caseosa. The large intestine contains much meconium. The 
humerus is 4.5 to 5 cm. long; the radius 3.7 cm.; the ulna 4 cm.; the 
femur, tibia, and fibula, each 4.2 to 4.6 cm. 

At the thirty-second week, the embryo is 39 to 41.5 cm. (15^ to 16^ 
in.) long, and weighs 1,500 to 2,500 gm. (48 to 81 oz.). The skin is 
lighter in color; the pupillary membrane has disappeared. The testicles 
are in the scrotum or the inguinal canal; the labia are still widely apart 
and the clitoris prominent. The nails reach nearly to the ends of the 
fingers. The humerus is 5 to 5.2 cm. long; the radius 4 to 4.2 cm.; 
the ulna 4.8 to 5 cm.; the femur 5.2 cm.; the tibia and fibula, each 4.8 
to 5 cm. The last sacral vertebra begins to ossify. 

At the thirty -sixth week, the embryo is 44.2 to 46 cm. (17.4 to IS 
in.) long, and weighs about 3.000 gm. (97 oz.). The scrotum begins to 
become wrinkled and the labia to close. The hair becomes more abun- 
dant, while the lanugo begins to diminish in amount. 

At the fortieth week, the foetus is fully developed and the term of its 
intra-uterine life accomplished. 

The fresh corpse of a new-born child at term no longer resembles that 
of the immature foetus. The skin is firm and pale, like that of an adult. 
The lanugo has disappeared except on the shoulders. In the majority 
of cases the hair on the head is 1.5 to 2 cm. (f to f in.) long. The great 



38 THE METHOD OF MAKING 

foutanelle is, in the average, 2 to 3 cm. (^ to 1 T V in.) long. As deter- 
mined by an analysis of 661 cases, the average length is 50 cm. (20 in.); 
the weight 3,256 gm. (105 oz.). The nails are hard and reach to the 
tips of the ringers, but not to those of the toes. The cartilages of the 
ears and nose are hard. The labia are more nearly closed. An ossifica- 
tion centre in the lower epiphysis of the femur should be sought for, as 
its presence is one of the most reliable signs of the maturity of the foetus. 
If it is absent, the foetus is, as a rule, not more than thirty-seven weeks 
old; but in rare cases it maybe absent at term. A centre of ossification 
1 mm. (.039 in.) in diameter indicates an age of 37 to 38 weeks, if the 
child was born dead or died soon after birth. Rarely it is no larger than 
this at term. A diameter, at birth, of 1.5 to 9 mm. (.058 to .351 in.) 
indicates an age of 40 weeks. A diameter of less than 9 mm. (.351 in.) 
indicates, as a rule, that the child has lived some time after its birth? 
a less diameter than 7 mm. (.273 in.), however, does not prove the con- 
trary. 

Twenty-four hours after the birth of the child, the skin is firmer and 
paler. The umbilical cord is somewhat shrivelled, although still soft and 
bluish in color. From the second to the third day, the skin has a yellow- 
ish tinge, and the cuticle sometimes appears cracked. The umbilical 
cord is brown and dry. From the third to the fourth day, the skin is 
yellower, and the cuticle is apt to separate from the skin. The umbili- 
cal cord is of a brownish-red color, flattened, semi-transparent, and 
twisted. The skin around its insertion is red and congested. 

The head should be examined for the marks of injuries. Very com- 
monly some portion of the scalp will be found swollen and infiltrated 
with blood and serum. This may be the caput succedaneum formed dur- 
ing delivery. The mouth and nose should be examined for the presence 
of any foreign bodies which might have caused suffocation. 

The neck should be examined for marks of strangulation. The um- 
bilical cord may be twisted around the child's neck and strangle it. The 
mark left by the cord is usually continuous, broad, not excoriated, some- 
times accompanied by ccchymoses in the skin. 

The entire body should be examined for the presence of vernix case- 
osa, blood, marks of injury, and the existence of putrefaction. It should 
be remembered that putrefaction is apt to commence earlier in the bodies 
of young children than in those of adults. 

The umbilical cord may be cut or torn. It usually separates by the 
fifth day, sometimes not until the tenth. If the umbilicus is cicatrized 
and healed, the child has probably lived for three weeks. A zone of 
redness around the insertion of the cord may exist previous to birth. 
Redness and swelling (which may disappear after death) with suppura- 
tion can only be found in a child which has lived for several days. The 
drying and mummification of the cord may take place as well in dead as 



POST-MORTEM EXAMINATIONS. 39 

in living children. It is possible for a child to die by haemorrhage from 
a cut or torn cord, either before or after it has breathed. 

The extremities may exhibit fracture of the bones. These may occur 
during intra-uterine life, from injuries to the woman or from unknown 
causes ; or may be produced by violence in delivery, or by injuries after 
birth. 

INTERNAL EXAMINATION. 

The Head. — The fontanelles and sutures should first be examined as 
to their size and for penetrating wounds. An incision should then be 
made through the scalp across the vertex, and the flaps turned backward 
and forward, as in the adult. With a small knife, the edges of the 
bones should be separated from the membranous sutures and the dura 
mater, beginning low down in the frontal and going back into the lamb- 
doidal suture on either side. The bones are then drawn outward and cut 
through around the skull, with strong scissors. The brain is removed 
and examined as in the adult. 1 

Effusions of blood — cephalhematoma — may be formed soon after 
birth, between the pericranium and bone, or, more rarely, between the 
dura mater and bone. Clots are also found between the dura mater and 
skull; between the dura and pia mater; more rarely in the substance of 
the brain, as the result of protracted or instrumental deliveries, or of 
injuries after birth. 

The cranial bones may be malformed, or exhibit the lesions of rickets 
or caries, or be indented, fissured, or fractured. These latter lesions 
may be produced during intra-uterine life by injuries to the mother, 
by unknown causes, by difficult deliveries, or by direct violence after 
birth. 

In cases of chronic internal hydrocephalus in young children in which 
the ventricles are much dilated and the brain substance thinned over the 
vertex, the brain is very apt to be torn in removal, and the amount of 
dilatation thus becomes difficult of determination. It is, therefore, 
better in such cases to place a pail of water beneath the head, or even 
immerse the latter in it, and remove the brain in the water. In this 
way, it floats after removal, supported on all sides. It may now be opened 
in the water and the extent of the lesion determined at once and parts 
saved for microscopical examination. 

If it be desired to preserve the brain for demonstration of the lesion 
or for a museum specimen, it should be transferred unopened to a large 
jar containing a mixture of equal parts of alcohol and water. A portion 
of the ventricular fluid should now be removed with a syringe provided 
with a small canula, and replaced by strong alcohol. This may be done 

1 Or an incision through the bones with a fine saw may be made as in the adult. 



40 THE METHOD OF MAKING 

by puncturing the ventricles from below. The fluid in the jar, as well 
as in the ventricles, should be changed in forty-eight hours and then 
gradually increased in strength until the organ becomes hard. The 
brain may then be cut transversely across, when the degree of dilatation 
of the ventricles, etc., will be revealed. The brain, of course, shrinks 
considerably by this process, but the relative proportions are approxi- 
mately preserved. 

The brain is normally much softer and pinker than in the adult, the 
pia more delicate; both may be much congested or anaemic without 
known cause. The ventricles contain very little serum. Malformations, 
apoplexies, hydrocephalus, simple and tubercular inflammatory lesions, 
are to be looked for. 

Spinal Cord. — Extravasations of blood between the membranes of 
the cord may occur from the same causes as those in the brain. Spina 
bifida is the most frequent malformation. 

The Thorax and Abdomen. — These are opened as in the adult. The 
peritoneal cavity contains a very little clear serum. A red fluid may be 
produced by decomposition. The peritoneum is often the seat of intra- 
uterine inflammation. 

The Diaphragm. — In still-born infants, its convexity reaches to the 
fourth or fifth rib. After respiration, it reaches a point between the 
fourth and seventh ribs. Its position is, however, so variable that it is 
of little diagnostic importance. 

The Ttiorax. — The thymus gland, at this period very large, occupies 
the upper portion of the anterior mediastinum, covering the trachea 
and large vessels. Its average weight is about 15.5 gm. (-J oz.). It is 
usually about 5 cm. (2 in.) long, 3.8 cm. (1-J- in.) wide at its lower 
part, and about .63 to .85 cm. (■£■ to J in.) in thickness. It may be 
hypertrophied and compress the large vessels, or be inflamed and sup- 
purating. 

The heart lies more nearly in the median line than in the adult. It 
weighs from 46 to 108 gm. (1-J to 3£ oz.). The ventricular walls are of 
nearly equal thickness. The pericardium contains very little serum. 
A considerable quantity of red fluid may accumulate here as a result of 
decomposition. There may be small extravasations of blood beneath the 
pericardium in still-born children and in those born alive. Pericardi- 
tis with effusion of serum and fibrin, and endocarditis with consequent 
changes in the valves, may exist before birth. Malformations and mal- 
positions of the heart cavities and large vessels are not infrequent. The 
time of closure of the foramen ovale and the ductus arteriosus varies 
very widely in different cases. 

The pleural cavities contain very little serum; but decomposition 
may lead to the accumulation of a considerable quantity of red fluid. 
Small extravasations of blood in the subpleural tissue may be found in 



POST-MORTEM EXAMINATIONS. 41 

children which have died before birth and after protracted labors. In- 
flammation, with exudation of serum, fibrin, and pus, may exist before 
birth. 

The lungs in a still-born child are small, do not cover the heart, are 
situated in the upper and posterior portion of the thorax, are of a dark- 
red color and of firm, liver-like consistence, and do not crepitate. In 
a child born alive, and which has respired freely, the lungs fill the 
thoracic cavity, but do not cover the heart as much as in the adult; they 
are of a light-red or pink color, and crepitate on pressure. If respira- 
tion has been incompletely performed, we find various intermediate con- 
ditions between the foetal and inflated states. 

If any doubt exists as to respiration having taken place, it is cus- 
tomary to employ the hydrostatic test. This is done by placing the 
lungs, first together, then separately, and afterwards cut into small 
pieces, in water. It is commonly said that if they sink, the child has 
not breathed; if they float, it has. This test is not, however, a certain 
one. Taylor says regarding it: 

1. That the hydrostatic test can only show whether a child has or has 
not breathed, not whether it was born alive or dead. 

2. That the lungs of children who have lived after birth may sink in 
water, owing to their not having received air, or to their being in a dis- 
eased condition. 

.3. That a child may live for some time with the lungs only partly 
inflated. 

4. That a child may live for twenty-four hours when no part of its 
lungs has been penetrated by air. 

5. The sinking of the lungs is no proof that a child has been born 
dead. 

6. That the lungs of children which have not breathed, and have 
been born dead, may float in water from putrefaction or artificial in- 
flation. 

The lesions of inflammation, and vesicular and subpleural emphy- 
sema, may be found in the lungs of new-born children. 

The pharynx should be opened and examined for foreign bodies. 

The larynx and trachea should be examined for the lesions of inflam- 
mation and for injuries to the cartilages. 

The thyroid gland weighs about 12 gm. ( 3 iii- ). It may be so en- 
larged as to interfere with respiration. 

The Abdomen. — The kidneys are lobulated and proportionately larger 
than in the adult. There may be ecchymoses on their surface; inflam- 
mation; deposits of uric acid and urates in the tubules of the pyramids; 
cystic dilatation of the tubules, sometimes reaching an enormous size. 
There may be absence or retarded development of one kidney. Malfor- 
mations and malpositions of the kidneys are of frequent occurrence. 



42 THE METHOD OF MAKING POST-MORTEM EXAMINATIONS. 

The suprarenal capsules are large. They may be dilated into large 
cysts filled with blood. 

The spleen is large and firm. It may be abnormally enlarged, and 
its surface is sometimes covered with fresh inflammatory exudations. 

The intestines : In the small intestines, inflammation and swelling 
and pigmentation of the solitary and agminated follicles are sometimes 
found. The large intestine usually contains meconium, but this may be 
evacuated before or during birth. The sigmoid flexure is not as marked 
as in the adult. 

The formation of gas in the stomach and intestines does not usually 
take place until respiration is established. If decomposition has com- 
menced, however, gas may be formed as a part of the process. 

The liver is of a dark-red color, is large, and contains much blood. 
Its size diminishes after respiration is established. The size is so vari- 
able, before and after respiration, that it gives little information as to 
the age of the child. Large extravasations of blood are sometimes found 
beneath the capsule of the liver, without known cause. A variety of 
pathological conditions, fatty and waxy degeneration, gummy tumors, 
etc., may be found. 

The bladder may be full or empty, both in still-born children and in 
those which have breathed. Dilatation and hypertrophy may exist dur- 
ing intra-uterine life. 

Generative Organs. — The external generative organs in both males 
and females are more prominent than in adults. The ovaries are high 
up in the pelvis and large; the cervix uteri is long; the body small and 
lax, resting forward against the bladder. Phimosis in the male is the 
normal condition. Malpositions and retarded development of the tes- 
ticles should be noticed. It should be observed whether the anus is per- 
forate. 

The Bones, in suspected cases, should be examined for the lesions of 
inflammation, rickets, and syphilis. 

Preservation. — The various foetal tissues may be preserved by the same methods 
as are employed for those of the adult; but as they are very delicate they should be 
handled with great care, and the preservative fluids changed with sufficient frequency. 



GEISTEEAL METHODS OF PEESEBVHsTG 

PATHOLOGICAL SPECIMENS AKD PEE- 

PAEESTG- THEM FOE STUDY. 



It is not our purpose in this section to give a complete account of the 
technical procedures required in the study of pathological specimens, 
since the methods are for the most part identical with those employed in 
the study of normal tissues, with which the student or practitioner is 
presumably familiar before prosecuting pathological studies. We wish 
simply to give a few brief hints as to the general methods which we have 
found most useful. Additional details will be found in parts of the book 
dealing with special tissues and organs. 

The Study of Fresh Tissues. — Although for the most part the con- 
ditions for the minute study of tissues are more favorable after they have 
been hardened in some preservative agent, it is yet in many cases very 
important to examine them in the fresh condition. For this purpose 
they may be teased apart in a one-half-per-cent solution of sodium chloride 
and mounted and studied in the same. The same solution may be used 
for studying semifluid substances, such 'as exudations from the mucous 
membranes, pus cells, etc. These preparations are not suitable for per- 
manent mounting, as they do not keep well. 

For staining the elements of fresh tissues, particularly the nuclei, 
and at the same time hardening them so that they can be mounted and 
preserved for some time, Carnoy's solution is of great value. It is 
made by adding to a saturated aqueous solution of methyl green, 1 per 
cent of acetic acid and -fa per cent of osmic acid. The tissue is immersed 
or teased in this solution, and after three to five minutes the color 
washed off and the specimen mounted in salt solution or in a mixture of 
equal parts of salt solution and glycerin. 

Thin sections of fresh tissues may be prepared by the use of some of 
the forms of the freezing microtome. That form devised by Thoma and 
made by Jung, of Heidelberg, is simple, cheap, and effective. 

Frozen sections may be stained in an aqueous solution of safranin 
and then mounted in a mixture of equal parts of glycerin and water. 

Decalcifying. — Bones which are the seat of lesions, or calcified tissues, 
must be freed from lime salts before thin sections can be made from 
them. This is best accomplished by the use of a saturated aqueous solu- 
tion of picric acid. The bone or other tissue should be cut into small 



44 GENERAL METHODS OF PRESERVING 

pieces, not larger than a cubic centimetre, and suspended by a thread in 
a large quantity of the fluid, which should have an excess of picric acid 
crystals at the bottom, and should be frequently shaken. Considerable 
time is required for decalcification by this method, but the results are 
better than by any other. 

If it be necessary to decalcify more rapidly, chromic acid may be used 
at first and the process completed by nitric acid. The small pieces of 
bone are suspended at first in a one-sixth-per-cent aqueous solution of 
chromic acid. After two or three days the strength of the solution is 
increased to one-quarter-per- cent and after three days to one-half-per- 
cent. After another week, the fluid should be changed and 1 per cent of 
nitric acid should be added. This fluid should be renewed every three 
days until the decalcification is complete, which may be determined by 
passing a fine needle through the specimen. The specimen should 
now be thoroughly soaked in water to remove all. traces of the acid, and, 
after lying for a day or two in strong alcohol, is ready for imbedding and 
section-cutting. 

Hardening and Preservation. — In the majority of cases, pathological 
specimens are best hardened first in Milllefs fluid and the process com- 
pleted by alcohol. Miiller's fluid is made by the following formula: 

Potassium Bichromate 2 parts 

Sulphate 1 " 

Water 100 " 

The specimens, which should be cut into small pieces, not more than 1 
or 2 om. square, are placed in a large quantity of the fluid, at least 
ten times the bulk of the specimen, and allowed to remain for two or 
three weeks. The fluid should be changed three or four times within 
the first ten days, and after this as often as the fluid becomes turbid or a 
sediment forms. After the specimens have acquired considerable con- 
sistency, or have been in the fluid for the proper time, they are removed 
from the fluid and soaked for from twenty-four to forty-eight hours in 
water, which should be frequently changed. They are then placed in 
equal parts of alcohol and water for forty-eight hours, and then in strong 
alcohol, by means of which the hardening is completed. They may be 
preserved in eighty-per-cent alcohol. 

For the special directions for hardening nerve tissues see page 15. 

DelafieUVs Osmic Acid Mixture. — This consists of 

One-per-cent solution of Osmic Aci'l 10 cc. 

One-fifth-per-cent solution of Chromic Acid 100 " 

Ninety-five-per-cent Alcohol ... .100 " 

Acetic Acid 1" 

After remaining for twenty-four hours in this solution, the specimens 
are transferred to eighty-per-cent alcohol, in which they may be perma- 



PATHOLOGICAL SPECIMENS. 45 

nently kept. This solution is very efficient in preserving the cells of the 
parenchyma of such organs as the kidney and liver in a nearly natural 
condition. 

Chromic Acid Mixture. — For many purposes a very excellent harden- 
ing may be obtained by using a mixture of one-sixth-per-cent aqueous 
solution of chromic acid 2 parts, and alcohol 1 part. This fluid, like all 
others, should be frequently changed, and the hardening may be finally 
completed with alcohol. This is commonly spoken of simply as the 
chromic acid mixture. 

If specimens are not in a good state of preservation, they will be best 
preserved by putting them at once into strong alcohol, which may be 
changed in two or three days. 

Although the above is the routine method of hardening tissues, de- 
partures from it are occasionally desirable in the preparation of different 
organs or for the accomplishment of special ends. Thus, in some cases — 
as in the kidneys, for example — the preservative fluids are brought into 
more direct and immediate contact with the tissue elements if they are 
injected under low pressure directly into the blood-vessels. Or by means 
of a hypodermic syringe the fluids may be thrown directly into the in- 
terstices of the tissue by thrusting the needle into them and slowly 
injecting the preservative agent. This is called interstitial injection. 

Osmic Acid is of great value for the hardeniug of small portions of 
delicate tissues, since it serves to fix the elements in a nearly normal con- 
dition and stains them of a brown or black color. It is generally used 
in one-per cent aqueous solution, the tissues being placed in it when quite 
fresh and allowed to remain for twenty-four hours. They are now washed 
in water and may be preserved in a mixture of equal parts of glycerin, 
alcohol, and water. Such preparations are best adapted for teasing or 
isolation by other methods than section-cutting. If it is desired to make 
sections of solid tissues preserved in osmic acid, the latter should be in- 
troduced by interstitial injection, and the fragment immersed in the acid 
for twenty-four hours, and then removed, washed, and placed in strong 
alcohol. Instead of using the one-per-cent osmic acid pure, very good 
results are obtained by diluting it with an equal volume each of water 
and strong alcohol. This is in many cases preferable, since the tissues 
are not stained so dark by the acid, and are more readily preserved sub- 
sequently in alcohol. 

Pathological specimens which occur, or are isolated in the form of 
membranes, should be stretched with pins on a piece of wood or flat cork 
before being immersed in the preservative fluids. 

Minute structures, such as occur in exudations from the mucous mem- 
branes and in cyst fluids, renal casts, etc., may be preserved by allow- 
ing them to settle, decanting as much of the fluid as possible, and then 
adding a considerable quantity of Muller's fluid, which after a few days 



46 GENERAL METHODS OF PRESERVING 

should be decanted and replaced by water. The latter should be renewed 
by decantation several times, and finally the sediment may be preserved 
in a mixture of equal parts of glycerin, water, and saturated aqueous 
solution of picric acid or alcohol. 

Imbedding and Section- Cutting. — Some dense tissues, after being 
well hardened, are sufficiently solid to permit of thin sections being made 
from them without further preparation, but in most cases very thin 
sections cannot be prepared without filling the interstices of the tissue 
with some imbedding material, which, gives it greater consistency and 
holds the tissue elements firmly in their natural relations to one another 
while the section is being made. Cacao butter, wax, paraffin, and vari- 
ous other substances have been largely used for this purpose, and are 
very useful ; but the more recently employed celloidin is by far the most 
valuable material, and may be used in nearly all cases. 

Celloidin, a non-explosive purified form of gun cotton, is best obtained 
in the form of thin shavings, since it is most easily dissolved in this 
form. A strong solution is made in equal parts of sulphuric ether and 
alcohol. The solution should have the consistency of thick molasses. 
The specimen, having beeu soaked for twenty-four hours in a mixture of 
equal parts of alcohol and ether, is placed in the celloidin solution, where 
it remains until permeated by it. This will ordinarily occur, if the speci- 
men be of moderate size, in from twelve to twenty four hours. For this 
preliminary soaking the celloidin solution may be a little thinner than 
above mentioned. If the specimen be small and require but little sup- 
port, it may now be laid directly on the end of a small cork, and a few 
drops of celloidin poured around it. In most cases, however, it is better 
to make a small paper box, in which the specimen is placed in a proper 
position, and the celloidin poured in around it so as to completely inclose 
it. In either case, a considerable quantity of celloidin should be poured 
around the specimen, since the celloidin shrinks considerably in harden- 
ing. If sections are to be cut with the microtome, the paper box should 
be made by winding a strip of filter paper around the end of a straight 
cork, allowing it to project for a sufficient distance beyond the end. The 
paper is held in place by tying a thread around it. We have thus a cy- 
lindrical box with a cork bottom which projects below it. It is better 
to use filter paper than sized paper, because the hardening of the celloi- 
din takes place more readily through it. 

After the specimen, either free on the end of the cork or in its box, 
is surrounded by celloidin, it should be allowed to stand for a short time 
exposed to the air, so that it may harden on the outside by the evapora- 
tion of the ether. If the temperature be high, the too rapid evaporation 
of the ether will cause bubbles to appear in the mass. This should be 
avoided by covering the specimen with a bell-jar. After the celloidin mass 
has acquired sufficient hardness on the outside to keep its shape, the. 



PATHOLOGICAL SPECIMENS. 47 

whole should be immersed in a mixture of equal parts of alcohol and 
water, in which the celloidin will harden and acquire a sufficient con- 
sistency for cutting in a few hours. When this is accomplished, the 
paper may be stripped off, and the specimen is ready for section-cutting. 
A little. practice will teach the operator of what consistency to make the 
celloidin solution, how long to expose to the air, etc. 

After the sections have been cut, they may be stained in the usual 
way (see below), and mounted in glycerin or balsam. If mounted in 
balsam, the oil of cloves, which is ordinarily used for clearing up the 
sections, will dissolve the celloidin. For some tissues this does no harm, 
since they are firm enough to hold together even in thin sections; but in 
handling friable and delicate tissues it is well to keep the celloidin in 
place, mounting it with the specimen, with the study of which it does 
not interfere. This may be accomplished by using the oil of origanum 
instead of oil of cloves for clearing. 

The uncut portion of tissue may be preserved, imbedded in celloidin, 
by keeping it in eighty-per-cent alcohol. 

Section- Cutting may be done by the free hand with a razor ground 
flat on the lower side, but better sections can be obtained by means of a 
microtome. One of the most useful of these is Thoma's, which is made 
of three sizes, the intermediate or the larger one being the more useful. 
The Schanze microtome is also well adapted for general work, as are some 
of the American instruments made on the same plan. 

Methods of Staining. — Sections of hardened tissues maybe stained 
for microscopical study in a variety of ways, but for routine work the 
double staining with hematoxylin and eosin is most generally useful and 
applicable to nearly all cases. 

The solution of hematoxylin is prepared as follows: To make 600 
c.c. of the solution, take 400 c.c. saturated solution of ammonia alum, 
and add to this 4 gm. crystallized hematoxylin (Merck's) dissolved in 
25 c.c. strong alcohol. This is exposed to the light in an unstoppered 
bottle for three or four days, when the color will gradually change from 
a dirty red to a deep bluish-purple color. The solution is now filtered 
and 100 c.c. each of glycerin and Hasting's wood naphtha are added. 
After standing for a day or two, the solution is filtered, allowed to 
stand for another day, and again filtered; and this is repeated until a 
sediment no longer forms in the fluid. 

The solution is now ready for staining, and should be considerably 
diluted with water as it is used, the best results being obtained by dilut- 
ing the fluid with from ten to twenty times its bulk of water. The sec- 
tions are placed in the fluid, and allowed to remain until they have 
acquired a distinct purple color which persists after rinsing in water. 
They are now placed for a moment in a dilute alcoholic solution of eosin, 
and then mounted in glycerin which has been colored lightly with an 



48 GENERAL METHODS OF PRESERVING 

alcoholic solution of eosin. In this way the nuclei of the cells will be 
stained of a purple color, while the cell bodies, and to a certain extent 
the intercellular substance, will be colored a light rose-red. 

If specimens are to be mounted in Canada balsam, they are stained 
with hematoxylin as before, and the eosin staining is done by tinging 
with eosin the alcohol with which the final dehydration of the specimen 
is accomplished. 

Methods of Preserving Specimens for Gross Demonstration and for 
Museums. — When specimens of diseased tissues or organs are to be pre- 
served entire for exhibition in jars in a museum, it suffices in most 
cases, after removing superfluous parts and making the requisite dissec- 
tion, to suspend them in proper position in jars containing thirty-per- 
cent alcohol. The alcohol should be changed as often as it becomes 
discolored by blood, and the specimens may be finally preserved in forty- 
per-cent alcohol. It is desirable that specimens which are to be exam- 
ined without removal from the jars should be placed in proper position 
before the alcohol is added, since when they are once hardened it is 
usually difficult to place them in good positions again; but this may be 
in most cases deferred for a day or two until a part of the blood is 
soaked out of them by the first dilute alcohol. The preliminary soak- 
ing to remove a part of the blood from specimens may be often advanta- 
geously done in strong brine. 

Cysts, such as ecchinococcus cysts, small embryos in their mem- 
branes, cystic kidneys, etc., may be preserved in a nearly natural condi- 
tion by placing them in a five-per-cent aqueous solution of chloral 
hydrate, and after a week replacing this by a ten-per-cent solution of 
the same, in which they may be permanently preserved. Such speci- 
mens are almost equally well preserved in a saturated aqueous solution 
of chloroform. 

Specimens which it is desirable to keep for a few days in a natural 
condition for the purpose of demonstration may be placed in the follow- 
ing solution: 

Water 1,000 c.c. 

Common Salt 100 gm. 

Saltpetre 25 " 

Carbolic Acid 5 " 

Glycerin 15 " 

Amylic Alcohol 50 

(Or^Ethylic Alcohol. . 100 ") 

This fluid is especially well adapted to the preservation of mucous 
membranes, such as that of the intestines, in a nearly natural condition 
for a few days. The specimens should be set in a cool place. 

We would most urgently commend to the reader the importance of 



PATHOLOGICAL SPECIMENS. 49 

putting pathological specimens which are to be hardened and subse- 
quently examined microscopically, at the earliest possible moment into 
the preservative fluids, which should always be abundant. And, further- 
more, when specimens are large, it is very desirable to cut them open, 
so that the fluids may come into direct contact with the tissues. It 
should be borne in mind that immediately after death or the removal of 
parts from the body, especially in warm weather, changes commence in 
the tissues and progress very rapidly, so that in some cases a few hours' 
or even a few moments' delay will not only render subsequent micro- 
scopical examinations difficult and unsatisfactory, but may lead to seri- 
ous errors. As above stated, Miiller's fluid and alcohol are the most gen- 
erally useful agents. Carbolic acid, glycerin, and usually chloral, 
should be avoided, and the not uncommon practice of wrapping a 
specimen in a cloth soaked in alcohol or carbolic acid, and permitting 
it to remain in this for hours or days, is of no use whatever in preserv- 
ing specimens of whieh microscopical examinations are to be made. 
Almost equally useless is the too common practice of placing a specimen 
in a bottle which it nearly fills, and pouring a little preservative fluid 
around it. Not only should the proper fluid be used, but it should be 
abundant, and the specimen so prepared and arranged that it may come 
into direct contact with it. 



part jr. 

CHANGES IN THE CIRCULATION OF THE 

BLOOD. 

CHANGES IN THE COMPOSITION OF THE 

BLOOD. 

DEGENERATIONS. 

ANIMAL PARASITES AND BACTERIA. 

INFLAMMATION. 

TUMORS. 



CHANGES I1ST THE CIRCULATION OE THE 

BLOOD. 



HYPEREMIA AND ANEMIA. 

There is an important series of changes in the character of the circu- 
lation during life which may, when death ensues, either alter considera- 
bly in appearance or disappear altogether. Among the more important 
of these changes are hyperc&mia— excess of blood in a part; and ancemia 
— deficiency of blood in a part. These conditionsTand the causes which 
lead to them will not be described in detail in this book, which has chiefly 
to do with alterations of the tissue which persist and may be studied 
after death. Tissues which have been the seat of a temporary, and 
sometimes of a prolonged, hyperaemia, may show to the naked eye nothing 
abnormal after death, or they may look redder than normal; they may 
be oedematous, and more blood than usual may flow from them when 
incised. On microscopical examination, the blood-vessels may be normal 
in appearance, or more or less distended with blood. Long-continued 
hyperaemia may lead to haemorrhage and transudation, to pigmentation, 
to a hypertrophy of tissue, or to an atrophy of tissue through pressure, 
or even to death of tissue. 

The paleness which is characteristic of anaemic tissues may not be 
evident after death. Anaemia may lead to no recognizable microscopical 
changes. On the other hand, if long continued it may induce atrophy 
and fatty degeneration, and, if excessive, may lead to death of tissue. 

HAEMORRHAGE AND TRANSUDATION. 

Haemorrhage is an escape of blood from the heart or vessels. It may 
occur from a rupture of the walls of the vessels, and is then called 
haemorrhage by rhexis. The rupture may be occasioned by injury, by 
some disease of the walls of the vessels which renders them too weak to 
resist the blood pressure from within, or it may occur from the blood 
pressure in the thin and incompletely developed walls of new-formed ves- 
sels in granulation tissue, tumors, etc. 

Under other conditions, without recognizable changes in the walls of 



54 CHANGES IN THE CIBCULATION OF THE BLOOD. 

the vessels, all the elements of the blood may become extravasated by 
passing, without rupture, through the walls of the vessels. This is called 
haemorrhage by diapedesis. These haemorrhages are usually small, but 
may be very extensive. They usually occur in the smaller veins and ca- 
pillaries, the cells and fluids of the blood passing out through the cement 
substance between the endothelial cells. Although no marked morpho- 
logical changes have as yet been detected which explain this extravasa- 
tion, it is probable that some change in the nutrition of the walls does 
occur which renders them more permeable. Haemorrhage by diapedesis 
is apt to occur as a result of venous congestion, or when the flow of 
blood in the smaller vessels has been suspended for some time; or it may 
result from the action of some poison, or from an injury not leading to 
rupture; or it may occur in incompletely developed blood-vessels, in 
tumors and other new-formed tissues. 

In the extravasation of blood by diapedesis, the white blood cells may 
pass through the walls of the vessels, partly at least in virtue of their 
amoeboid movements; the red cells, on the other hand, having no power 
of spontaneous movement, are, according to Arnold, carried passively 
through the walls by minute currents of fluid which, under the changed 
condition, stream in increased force and volume through the endothelial 
cement substance into the lymph spaces outside. 

The altered condition of the blood-vessels leading to haemorrhage may 
be local or general, and in the latter case it may either be congenital, as 
in some cases of the haemorrhagic diathesis, or it may be the result of 
some general disease, as scurvy, purpura, etc. The presence of bacteria 
in the vessels, as in malignant endocarditis and in haemophilia neona- 
torum, is believed in some cases to produce changes in the walls of the 
vessels, leading to extravasation. 

Yery small haemorrhages are called petechia ; larger, diffuse accumu- 
lations of blood in the interstices of the tissues are commonly called 
ecchymoses or suggillations. A complete infiltration of a circumscribed 
portion of tissue with blood is called a hcemorrhagic infarction. A col- 
lection of blood in a tumor-like mass is called a hcematoma. Sometimes 
the elements of the tissue into which the blood escapes are simply crowded 
apart; sometimes, as in the brain, they are broken down. 

The extravasated blood in the tissues usually soon coagulates, although 
exceptionally it remains fluid for a long time. A certain number of the 
white blood-cells may wander into adjacent lymph vessels, or they may 
remain entangled with the red cells in the meshes of the fibrin. The 
fluid is usually soon absorbed; the fibrin and a portion of the white 
blood-cells disintegrate and are absorbed. The red blood-cells soon give 
up their haemoglobin, which decomposes, and may be carried away or be 
deposited either in cells or in the intercellular substance at or near the 
seat of the haemorrhage, either in the form of yellow or brown granules 



CHANGES IN THE CIRCULATION OF THE BLOOD. 55 

or as crystals of hsematoidin. Sometimes all trace of extravasations of 
blood in the tissues disappears, but frequently their seat is indicated for 
a long time by a greater or less amount of pigment, or by new-formed 
connective tissue. Occasionally the blood-mass, in a more or less degene- 
rated condition, becomes incapsulated by connective tissue, forming a 
cyst. 

Transudation is the passage, through the walls of the blood-vessels 
into the lymph spaces outside, of fluid from the blood, with little or no 
admixture of its cellular elements. This occurs constantly, to a certain 
extent, under normal conditions, and forms the commencement of the 
lymph circulation. But when the amount of fluid passing through the 
walls of the blood-vessels is increased, or its outflow into the larger lymph 
trunks is hindered so that it accumulates in undue quantity in the inter- 
stices and lymph channels of the tissues, the condition is pathological 
and is called transudation. An accumulation of transuded fluid in the 
interstices of the tissues is called oedema; in the serous cavities, dropsy. 
Its occurrence is usually dependent upon some hindrance to the venous 
circulation or upon some change in the condition of the blood, which 
may become more watery or lead to alterations in the walls of the blood- 
vessels. A simple interference with the outflow of lymph does not usually 
alone suffice to induce transudation, although it may favor its occurrence. 
The transuded fluid is usually transparent and colorless or yellowish; it 
contains the same salts as the blood plasma, but less albumen. It may 
contain fat, mucin, urea, biliary acids, coloring matter of the bile; fibri- 
nogen is usually present in variable quantity, and rarely fibrin. It may 
contain endothelial cells from the lymph spaces, and a variable number 
of red and white blood-cells. The amount of fluid which may accumu- 
late in the tissues varies greatly, depending upon whether they are loose 
or dense in texture. The fibres and cells of loose tissues may be crowded 
widely apart; the cells are apt to be more granular than normal, and may 
be atrophied. Transudations occurring in inflammation usually contain 
a considerable number of white blood-cells and more or less fibrin, and 
differ in this from the non-inflammatory transudations; but there is no 
sharp distinction in some cases between them. The inflammatory trans- 
udations are often called exudations. 

THROMBOSIS AND EMBOLISM. 

Thrombosis. — -Thrombosis is a coagulation of blood in the heart or 
vessels during life. The coagulum is called a thrombus. Thrombi may 
lie against the wall of a vessel, only partially filling the lumen, and are 
then called parietal thrombi ; or they may entirely fill the vessel, and 
are then called obliterating thrombi. 

Thrombi may occur as the result of an injury to the wall of a vessel, 
or may follow its compression or dilatation; they may result from some 



56 CHANGES IN THE CIRCULATION OF THE BLOOD. 

alteration of the wall of the vessel by disease or by the retardation of 
the circulation. So long as the endothelial linings of the vessels are in- 
tact, simple retardation of the circulation does not usually alone suffice 
to induce coagulation; but changes in the endothelium from a great 
variety of causes, such as inflammation, degeneration, atheroma, calcifi- 
cation, and the presence of tumors and foreign bodies, favor its occur- 
rence. 

Thrombi maybe composed of fibrin and of red and white blood-cells, 
intermingled in about the same proportion as in an ordinary extravascu- 
lar blood-clot. These are called red thrombi, and usually occur from 
some sudden stoppage of the circulation. Other thrombi, usually such 
as form while the blood is in motion, may consist almost entirely of 
white blood-cells with a little fibrin, or of these intermingled with blood- 
plates, or they may consist almost entirely of blood-plates; all of these 
forms are called white thrombi. Bed thrombi, when decolorized by 
changes in the blood-pigment, may somewhat resemble genuine white 
thrombi. Mixed thrombi are usually lamellated, and contain varying 
proportions of fibrin and red and white blood-cells. 

The changes which occur in the thrombus after its formation may be 
either in the direction of degeneration or organization. In some cases 
they seem to undergo a simple shrinkage and decolorization. The 
leucocytes, the fibrin, and the blood-plates may degenerate, forming a 
granular material which may become infiltrated with salts of lime, form- 
ing the so-called phleboliths, or vein-stones ; in other cases, the thrombi 
may soften and disintegrate. Certain thrombi contain bacteria or other 
infectious material, and on softening of the thrombus these may be 
carried into the circulation, producing very disastrous results. Finally, 
the thrombus may be replaced by a new formation of vascular connective 
tissue, itself disappearing as the new tissue is formed. This is called 
organization of the thrombus, but in reality the new connective tissue is 
produced, in large measure at least, not from the cells of the thrombus 
itself, but from the cells of the walls of the affected vessel, from whose 
vasa vasorum the new blood-vessels of the thrombus also arise. It is 
possible, however, that the white blood-cells of the thrombus may con- 
tribute somewhat to the formation of the new tissue. In this way, the 
vessel may be completely and permanently occluded, or, more rarely, a 
channel may be re-established through the new connective-tissue mass. 

Thrombi in veins may lead to hyperemia and oedema; in arteries, to 
an ansemia whose significance will vary greatly, depending upon the sit- 
uation of the occluded vessel. 

Embolism. — This is the stoppage of a blood-vessel by the arrest in its 
lumen of some material carried along in the circulating blood. The 
substance causing the stoppage is called an embolus. This may be 
composed of a great variety of substances. The most common emboli 



CHANGES IN THE CIRCULATION OF THE BLOOD. 57 

are detached portions of thrombi, and these may have all the variety of 
structure which thrombi present. Masses of bacteria or other parasites, 
fragments of the heart valves and of tumors, droplets of fat from the 
medulla of fractured bones, masses of pigment, bubbles of air, etc., may 
form emboli. Embolism is, in a majority of cases, confined to the 
arteries and to the branches of the portal vein. 

The primary effect of the stoppage of an arterial trunk is, of course, 
to largely deprive the region of the body to which its branches are dis- 
tributed of its normal supply of blood. If the branches of the occluded 
artery form anastomoses with other arteries beyond the point of stop- 
page, a collateral circulation may be established and the embolus do no 
harm. If, however, the occluded vessel be a so-called terminal artery, 
that is, one whose branches do not form anastomoses with other arteries, 
the result of the embolism is quite different. When a terminal artery is 
occluded by an embolus, the tissue of the affected region usually dies, 
and there may be an extravasation of blood by diapedesis, leading to the 
formation of a dark-red, solidified area called a hemorrhagic infarc- 
tion. 1 The area of infarction corresponds to the region supplied with 
blood by the occluded vessel, and is usually more or less wedge-shaped. 

After a time, the infarction becomes decolorized; inflammatory 
changes may occur in its periphery, the blood and involved tissues may 
undergo degeneration and be absorbed, and finally the seat of the infarc- 
tion may be indicated only by a mass of cicatricial tissue, which fre- 
quently contains more or less pigment. 

In another class of cases, instead of an extravasation of blood in the 
affected region, the tissue is simply deprived of nourishment and under- 
goes necrosis. The affected area is then usually light in color, and is 
called a white infarction. Inflammatory changes may occur in its 
periphery, and a new connective-tissue capsule form around it, and the 
dead mass may thus persist for some time, or be gradually absorbed and 
replaced by cicatricial tissue. The scope of this book does not permit 
us to consider the somewhat complicated and often obscure reasons why 



1 When an embolus lodges in a terminal artery, and the circulation in the territory 
supplied by its branches ceases, the pressure from the side of the artery is reduced to 
zero; but, on the other hand, according to Cohnheim, the venous pressure now makes 
itself felt in a backward direction, and the capillaries and small veins in the affected 
region become crowded with blood. This blood is stagnant, however, and the walls 
of the small vessels, being deprived of their usual nourishment, undergo, it is believed, 
degenerative changes which favor the occurrence of extensive diapedesis. Thus, in 
the hemorrhagic infarction, not only the blood-vessels but the extra vascular tissues 
also are crowded with stagnant blood. The researches of Litten make it seem prob- 
able that, in most cases, the back pressure in the region of infarction comes, not from 
the veins, or not from them alone, but from adjacent arterial twigs which communi- 
cate with the capillaries of the affected region. 



58 CHANGES IN THE CIRCULATION OF THE BLOOD. 

in one case we have haemorrhagic, in another white infarction, as a 
result of embolus. 

If the embolic material consists of or contains infectious substances, 
such as some forms of bacteria, in addition to the mechanical effects of 
simple emboli, we may have gangrene, suppuration, and formation of 
abscesses, etc., as the result of the local action of the infectious material, 
even though this may be present in very small amount. 

The organs in which embolic infarctions most frequently occur are 
the spleen, kidney, brain, lungs; less frequently the retina, liver, and 
small intestines. Haemorrhagic infarctions are not liable to occur in 
the liver from emboli in the branches of the portal vein, on account of 
the blood-supply which may come to the affected region through the 
branches of the hepatic artery. On the other hand, embolic abscesses 
from infectious emboli are of not infrequent occurrence here. Haemor- 
rhagic infarctions may occur exceptionally in regions not furnished with 
terminal arteries, as in the small intestines. 



CHANGES I]ST THE COMPOSITION OF THE 

BLOOD. 



Only the more common morphological alterations of the blood will 
be considered here, and particularly such as may be appreciable after 
death. 

The coagulability of the blood and the characters of the resulting clot 
vary widely, depending partly upon the composition of the blood and 
partly upon the conditions under which the coagulation occurs. There 
may be very little coagulation of the blood in death, from the exclu- 
sion of air from the lungs, or from diseases and accidents which in 
any way interfere with the aeration of the blood and permit the accu- 
mulation of carbonic acid within it. Thus, in death from strangulation 
or drowning, many chronic diseases, scurvy, and under many conditions 
which we do not understand, the blood may remain fluid, or nearly so, 
after death. On the other hand, in a variety of acute inflammatory dis- 
eases, such as rheumatism, pneumonia, etc., very voluminous clots may 
be formed, although this is by no means constantly the case. The fact 
that large clots form after death is not conclusive evidence that an un- 
due amount of fibrin-forming elements were present in the blood, nor 
does the absence of marked coagulation prove a diminution in the blood 
of fibrin-forming elements. 

The blood may be very thick from the removal of its fluid consti- 
tuents, in diseases associated with excessive serous discharges from the 
intestines. It is especially marked in some cases of cholera, and is called 
anhydrmmia. On the other hand, the blood may contain a large amount 
of water in proportion to its solid ingredients — albumen and blood-cells. 
This is called hydrcemia, and occurs in a variety of diseases of the heart, 
kidneys, liver, and lungs. In anaemia, etc., the blood looks more or less 
watery. 

There may be a diminution in the number of the red blood-cells and 
in their haemoglobin content, as well as changes in their shape. This 
may be seen in various forms of aucemia. The red blood-cells may be 
unduly pale from a decrease in the amount of haemoglobin. Varying 



60 CHANGES IN THE COMPOSITION OF THE BLOOD. 

numbers of spheroidal or irregular-shaped bodies, smaller than the red 
blood-cells but having the same color, may be found, particularly in 
marked cases of pernicious anaemia. These are called microcytes and 
may be ill-developed red blood-cells or red blood-cells in a degenerated 
condition. The number of red blood-cells in extreme cases of anaemia 
maybe diminished to one-tenth of the normal or to about 500,000 in the 
cubic millimetre. Under these conditions the white blood-cells may re- 
main in normal proportion or they may be increased in number. Fatty 
degeneration of the heart and blood-vessels, liver, kidney, etc., and 
capillary haemorrhages and a change of the yellow into red marrow, are 
frequent accompaniments of excessive anaemia. This latter change is 
largely due to the disappearance of the fat. Nucleated red blood-cells 
are also observed in the red marrow. 

Leucocytosis signifies a temporary increase in the number of white 
blood-cells, and this is usually of moderate amount. It occurs in a 
variety of acute inflammatory diseases, in profuse suppuration in any 
part of the body, often in connection with cancerous growths, tuber- 
culosis, etc., and may, as above stated, be associated with anaemia. 

Leukcemia (Leucocythcemia). — This disease is characterized by a 
persistent, progressive, and often enormous increase in the number of 
the white blood-cells. The blood is pale in well-marked cases, but not 
watery, and the number of white blood-cells may in extreme cases equal 
or even exceed that of the red. There are sometimes nucleated cells in 
the blood, of irregular shape and larger than the leucocytes, and others 
which are smaller. The origin of these cells is not yet certain; the leu- 
cocytes are frequently in a condition of fatty degeneration. There may 
be a decrease in the number of red blood-cells in leucocythaemia. There 
are marked changes in the liver, spleen, and lymph glands, as well as in 
the bone marrow, in leukaemia; the degree of involvement of the dif- 
ferent organs varying in different cases (see Leukaemia, in section de- 
voted to general diseases). 

Most of the above-mentioned changes in the morphological characters 
of the blood are better studied during life than after death, since the 
redistribution of its elements, owing to the clotting and the effects of 
gravity, renders the obtaining of a pure sample very difficult or impos- 
sible, and the results of examination only in a very general way reliable. 

Melancemia. — In this condition, the blood contains larger and smaller 
irregular-shaped particles or masses of brown or black pigment. This 
condition is most frequently the result of intermittent and remittent 
fever, particularly the severer forms. It may be accompanied by anaemia 
and leucocytosis. It does not occur in all cases of the above-named affec- 
tions. It may be transient in character. The pigment may be free, or 
more usually is inclosed in leucocytes. Under the same conditions, 
pigment may be deposited in the liver, spleen, lymph glands, bone 






CHANGES IN THE COMPOSITION OF THE BLOOD. 61 

marrow, and blood-vessels. Owing to the deposit of pigment in the 
organs, they may assume a gray or slate color. The pigment is sup- 
posed to originate in the decomposition of the haemoglobin. 

Pigment which has been taken into the lungs from the air, such as 
coal-dust, etc., may find its way into the blood either before or after 
deposition in the bronchial or other lymph glands, and may be after- 
wards deposited in the spleen and liver. 

Foreign Bodies in the Blood. 

Various bodies which do not belong there, aside from those above 
mentioned, may find access to the vessels and mingle with the blood. 
Pus cells may get into the blood from the opening of an abscess into the 
vessel, or from some inflammatory change in its walls. Desquamated 
endothelial cells from the vessel walls, either in a condition of fatty de- 
generation or in various stages of proliferation, may be mingled with the 
normal blood elements; also tumor cells of various kinds, fragments of 
disintegrating thrombi, portions of heart valves, etc. Crystals of biliru- 
bin have been found in the blood in icterus. 

Fat, in a moderate amount, is a normal ingredient of the blood dur- 
ing digestion and in lactation. Under pathological conditions it may 
occur in larger and smaller droplets. Lipcemia occurs as a result of 
deficient oxidation, in diabetes, in drunkards, and in some cases of 
dyspnoea from various causes. The droplets are small and liable to escape 
observation. 

In many cases of injury, particularly in crushing fractures of the 
bone, the fat of the marrow finds its way into the blood, and it may col- 
lect in large drops in the vessels of the lungs, forming the so-called fat 
emboli, or it may pass the lungs and form emboli in other parts, as the 
brain, kidneys, etc. Fat embolism in eclampsia is of occasional occur- 
rence. 

The fat may be absorbed from the vessels, having produced little or 
no disturbance; or in some cases it may produce serious results by the 
stoppage of a large series of vessels in the lungs, brain, or other parts of 
the body. 1 The fat may be best seen by cutting sections of the fresh 
tissues with the freezing microtome and staining them at once for twenty- 
four hours with one-per-cent aqueous solution of osmic acid. They may 
then be mounted in glycerin. 

Air in the Blood, as the result of an opening in the veins, is of occa- 
sional occurrence. If the amount of air be small, it appears to be readily 
absorbed and does little or no harm. If, on the other hand, a large 
quantity is admitted to the veins at once, it collects in the right side of 

1 Consult for resume of this subject, with good bibliography, article by Park on 
" Fat Embolism," New York Med. Jour., Aug. 16th, 1884. 



62 ( CHANGES IN THE COMPOSITION OF THE BLOOD. 

the heart, from which the contractions of the organs are unable to force 
it in any considerable quantity, and, the supply of blood being thus cut 
off from the lungs, death very quickly ensues. It is especially from 
wounds of the veins of the neck and thorax that the accident is most apt 
to occur. But it may be due to the introduction of air into the uterine 
veins in intra-uterine injection, or in the removal of tumors. 1 

The occurrence of animal and vegetable parasites is considered more 
in detail in parts of this book devoted to these organisms. It will suffice 
to mention here that the more important of the animal parasites of the 
blood are: the Filar ia sanguinis hominis, the Distoma haematobium, and 
the embryos of trichina and echinococcus, which are of occasional and 
usually temporary occurrence. 

The various species of bacteria which may be found in the blood will 
be considered in parts of this book in which these organisms are treated 
in detail. 2 

1 Consult Couty, " Etudes exp. surl'entree de l'air dans les veiDes," Paris, 1875, for 
experiments and older literature; also later article by Couty, Arch, de Physiol, nor. et 
path., 2d ser., T. 4, p. 429, 1877. More recent consideration of the subject in Archiv 
fur klin. Medicin, Bd. 31, p. 441, 1882, by Jurgensen. 

2 For literature and detailed consideration of morphological and other alterations of 
the blood, consult Cohnheim, " Vorlesungen iiber allgemeine Pathologie," Bd. I., 2d ed., 
or Orth, ' ' Lehrbuch der speciellen pathologischen Anatomie," or Birch- Hirschf eld, 
" Lehrbuch der pathologischen Anatomie," 3d ed., Bd. II. For methods of blood ex- 
amination for clinical purposes, consult Bizzozero, " Handbuch der klinischen Mikro- 
scopie," translation into German by Lustig and Bernheimer, or Jaksch, " Klin. Diag- 
nose," 2d ed., 1889. 

For method of blood counting, apparatus, etc., consult Freeborn, "Histological 
Technique," in Wood's " Handbook of the Medical Sciences." 



DEGENERATIVE CHANGES IN THE TISSUES. 



Necrosis. — Necrosis is the death of a circumscribed portion of tissue. 
It may be the result of insufficient nutrition from the cutting off of the 
blood supply; or it may depend upon the action of destructive chemical 
agents, extreme degrees of temperature, certain materials produced by 
the life processes of some forms of bacteria; or it maybe due to mechani- 
cal injury. The appearances which dead tissues present under the mi- 
croscope vary greatly. In some cases, we have a simple and gradual dis- 
integration and softening of the tissue, resulting in a mass of degenerated 
cells and cell detritus, with more or less fluid and various chemical 
substances resulting from decomposition. The softening of the brain in 
embolism is an example of simple necrotic softening. In some cases, 
the- dead tissues simply gradually dry and shrivel and become hard and 
dark colored. 

In another class of cases, the dead tissues are permeated by fluids 
which may be dark red in color from the solution of coloring matter 
from the blood, and contain bacteria which induce putrefaction with 
the production of gases and various new chemical substances. The 
tissues become swollen and granular, and disintegrate ; and finally the 
whole may form a mass of irregular granules with fat droplets, various 
forms of crystals, shreds of the more resistant kinds of tissue, and 
bacteria. 

Coagulation Necrosis. — If the supply of blood is shut off from a por- 
tion of tissue which is surrounded by, or continuous with, other tissue 
in which the blood continues to circulate, there results a death and trans- 
formation of a peculiar character. The composition of the cells of the 
tissue is altered so that the cell bodies are shining and translucent, di- 
minished in size, sometimes altered in shape, and the nuclei of the cells 
disappear. The white infarctions of the spleen and kidneys, the areas 
of coagulation necrosis in phthisis, and the pseudo-membrane in croup- 
ous inflammation of the mucous membranes are the most common ex- 
amples of this lesion. 

If, for example, in the spleen, one of the small arteries is plugged by 
au embolus, a corresponding portion of the spleen becomes anaemic and 



64: DEGENERATIVE CHANGES IN THE TISSUES. 

appears as a white, wedge-shaped mass, sharply defined from the sur- 
rounding splenic tissue. If such a white infarction has existed but a 
short time, there is hardly any difference between the appearance of its 
anatomical elements and those of the surrounding spleen, except that 
they are differently affected by staining fluids. If the infarction is 
older, the cells are small and shiny and their nuclei cannot be seen. 

In croupous inflammations of mucous membranes, the epithelial cells 
become shiny, the nuclei disappear, and the shape of the cells is changed 
by the coagulation necrosis so that a number of them together often look 
like a network of coagulated fibrin. 

Cheesy Degeneration. — As commonly used, this term embraces the 
changes in the tissues which we have just considered under the more 
appropriate name of coagulation necrosis. But it is also and more 
properly applied to that form of degeneration in which^ under a variety 
of conditions, the dead tissue elements lose their normal structural 
features and become converted into an irregularly granular albuminous 
and fatty material which sometimes tends to disintegrate and soften, 
sometimes dries and becomes dense and firm, or may become infiltrated 
with salts of calcium. Thus cheesy degeneration may, and very often 
does, occur in tissues which are in the condition of coagulation necrosis, 
but it also occurs in tissues which are not the seat of coagulation necro- 
sis, but which, for a variety of reasons and in a variety of ways, have lost 
their vitality. 

The terms coagulation necrosis and cheesy degeneration, as commonly 
used, in part actually cover the same degenerative conditions in the 
tissues. Both are indefinite, and will no doubt remain so until we ob- 
tain a more definite knowledge of the lesions which they represent. 

Parenchymatous Degeneration (cloudy swelling). — In this condition, 
the cells of tissues and organs are swollen and filled with small albu- 
minous granules which may be so abundant as to entirely conceal the 
original cell structure. The granules disappear on treatment with acetic 
acid, and are insoluble in ether. This degeneration may be present in 
the parenchyma cells of any inflamed organ, but is most marked and 
frequent in the liver, kidney, heart-muscle, and mucous membrane of 
the gastro-intestinal canal. It may occur in infectious or severe febrile 
diseases, after severe burns, and in poisoning with arsenic, phosphorus, 
or mineral acids. The cells in a condition of parenchymatous degenera- 
tion may regain their normal condition, or become fatty, or disintegrate. 
In such organs as the liver, kidney, and heart, the gross appearances are 
often very characteristic ; the tissue is swollen and has a less translucent 
and more dull and grayish look than under normal conditions. 

The microscopical study of this lesion is best done in sections of the fresh tissue 
made with the freezing microtome, or in teased fresh tissue in one-half -per-cent salt 
solution. 



DEGENERATIVE CHANGES IN THE TISSUES. 65 

Fatty Degeneration. — This is the conversion of the protoplasm of 
cells into fat, which accumulates in the cell body. The fat is usually 
present in the cell in very small particles or droplets, but these may 
coalesce to form large drops. The protoplasm may even be almost en- 
tirely replaced by the fat. 

Fatty Infiltration of cells is a common occurrence under normal as 
well as pathological conditions. The fat is believed to originate outside 
of the cells and simply accumulate in them, causing a passive atrophy 
of the protoplasm. In this way fatty infiltration is believed to differ 
essentially from fatty degeneration, but in many cases a definite distinc- 
tion between the two is impossible with our present knowledge of the 
chemistry of cell life. In general, the fat droplets are larger in fatty in- 
filtration than in fatty degeneration, yet to this there are many excep- 
tions. Fat granules and droplets are recognized in cells by their strong 
refraction, by their solubility in alcohol and ether and their insolubility 
in acetic acid, and by the black color which they assume when the fresh 
tissue is treated with osmic acid. ISTot infrequently feathery clusters of 
delicate fat crystals occur within the cells. Fatty-degenerated cells may 
break down and form an oily detritus, in which, especially when much 
moisture is present, cholesterin crystals may be formed by decomposition 
of the fat. 

To the naked eye, organs in a condition of marked fatty degeneration 
are usually larger and softer than normal, have a grayish yellow color or 
are mottled with yellowish streaks or patches, and the normal markings 
of cut surfaces are more or less obscured. 

Fatty degeneration may be due to local or general disturbances of 
nutrition, from a great variety of causes — disturbances which either 
directly affect the life processes of the cells themselves, or which produce 
alterations in their nutritive supply. In addition to its local occurrence, 
as a result of local disturbances of circulation, in the vicinity of inflam- 
mations or in tumors, etc., it is apt to occur in the liver, heart-muscle, 
and kidne}^ in chronic exhausting diseases and in conditions and diseases 
to which profound anaemia is incident, or as the result of the action of 
certain poisons, such as phosphorus and arsenic. Fatty degeneration is, 
as a rule, a more serious lesion than fatty infiltration.] 

Tissues in a condition of fatty degeneration or infiltration may be studied by teas- 
ing, or cutting the fresh tissue with the freezing microtome and examining unstained, 
or lightly stained with eosin, in one-half -per- cent salt solution. Or they may be placed, 
when fresh, for twenty-four hours in one-per-cent solution of osmic acid, and then 
studied, either after teasing or in sections, in glycerin. A preliminary hardening in 
Muller's fluid and afterwards in alcohol gives moderately good results if the lesion is 
extensive. But it should be remembered that in tissues which have been soaked in 
alcohol the fat is no longer present, its former seat being indicated by clear spaces 
which are filled with the mounting medium. The fat crystals, however, often persist 
after prolonged soaking in alcohol. 
5 



DO DEGENERATIVE CHANGES IN THE TISSUES. 

Amyloid Degeneration (waxy or lardaceous degeneration). — This is 
a process by which the basement substance of various forms of connective 
tissue, and especially the walls of the blood-vessels, become swollen and 
thickened by their conversion into a translucent, firm, glassy, colorless 
material, albumin on s in character. This albuminous material may be 
present in the tissues in such small amount as to be recognizable only 
under the microscope, or it may be so abundant as to give a very char- 
acteristic appearance to the tissue. Parts in which the lesion is marked 
are usually larger and contain less blood and feel harder than normal, 
and have a peculiar dull shining and translucent appearance which varies 
in character, depending upon the extent and distribution of the degen- 
erated areas and upon its association with other lesions, such as fatty 
degeneration. .It most frequently occurs in the smaller arteries and 
capillaries, whose lumen becomes encroached upon by the thickening of 
the walls which the process involves. It is usually the media and inter- 
mediary layers of the inti ma which are earliest and most extensively 
affected. The change also often occurs in the interstitial connective 
tissue and membranse propriae of organs and in reticular connective 
tissue. It is both asserted and denied that it may affect the parenchyma 
cells of organs. We have not been able to find unmistakable evidence of 
its occurrence in parenchyma cells. These, however, frequently undergo 
atrophy as the result of pressure from the swollen, degenerated tissue. 

It is not yet known whether amyloid degeneration is due to a direct 
transformation of the tissue, or is an infiltration of the tissue by some 
abnormal material formed elsewhere and brought to it, or is derived 
from the blood. 

Amyloid degeneration occurs most frequently and abundantly in the 
liver, spleen, kidneys, intestinal canal, and lymph glands; but it may 
occur, usually in a less marked degree, in other parts of the body: in 
the larger blood-vessels, in the interstitial tissue of the heart and mucous 
membranes of the air passages, and in the generative organs. It may 
occur locally or appear in various parts of the body at once. It may 
exist without any known cause, but it most frequently occurs in con- 
nection with severe wasting diseases, particularly in those involving 
chronic suppuration and ulceration, especially of the bones. It fre- 
quently occurs in tuberculosis, syphilis, in the cachectic condition in- 
duced by malignant tumors, and is occasionally seen in severe malarial 
infection, dysentery, and leukaemia. 

For microscopical examination, the tissue, either fresh or after preservation, should 
be cut into thin sections, and these deeply stained with one-per-cent aqueous solution 
of methyl violet; the sections are washed in water and mounted in glycerin. The dif- 
ferentiation between the amyloid and other parts is more distinct if, after staining, 
the specimen be dipped for an instant in HC1 and alcohol 1 : 100, and then carefully 
rinsed, before mounting in glycerin. The degenerated areas are thus stained rose red, 



DEGENERATIVE CHANGES IN THE TISSUES. 67 

while the normal tissue elements have a bluish-violet color. In some cases, for reasons 
which we do not know, the amyloid substance does not show a well-marked reaction 
with methyl violet. Other aniline dyes also differentiate amyloid substance from 
normal tissues. On treating sections of amyloid tissue with solution of iodine, the 
degenerated parts acquire a mahogany color. If they are then treated with sulphuric 
acid, the degenerated portions acquire a greenish or blue color ; but the latter reac- 
tion is not very reliable. 

Corpora Amylacea are small, spheroidal, homogeneous or lamellated 
bodies which assume a bluish color on treatment with solution of iodine 
or iodine and sulphuric acid. They are frequently found in the acini 
of the prostate gland, sometimes in large numbers; in the ependyma 
of the ventricles of the brain, and in areas of sclerosis of the brain and 
cord; also in extravasations of blood and in various other situations. 
They may occur under normal as well as pathological conditions, and 
are apparently of little importance. They seem to have nothing to do 
with amyloid degeneration, although they somewhat resemble its pro- 
ducts. Some of the tube-casts of the kidney resemble in many respects 
the corpora amylacea. 

Mucoid Degeneration may occur in cells or in intercellular substance. 
When occurring in cells, it consists, under pathological as under normal 
conditions, of the transformation of the protoplasm into a translucent, 
semi-fluid material, occupying more space than the unaltered proto- 
plasm, and hence causing a swelling of the cells. This new-formed 
material contains mucin in solution, which is precipitated by acetic 
acid. It occurs under a variety of conditions, sometimes as a morbid 
increase of a normal function of cells, as in many catarrhs, sometimes 
as an entirely abnormal transformation. The cells may be entirely 
destroyed by the accumulation of the mucoid material within them. 

In certain cases, as in many tumors, in cartilage, bone, and other 
tissues, the intercellular substance undergoes conversion into mucin- 
containing material, losing almost entirely its original structure. The 
cells in such cases may be affected only secondarily by the pressure which 
the new-formed material exerts upon them. 

Colloid Degeneration is very closely allied, both in chemical and 
morphological characters, to mucoid degeneration, and in many cases 
there is no definite microscopical distinction between them. But colloid 
material is firmer and more consistent than mucous, does not yield a pre- 
cipitate on addition of acetic acid, and its formation is usually confined 
to cells; not involving intercellular substance, except by an atrophy 
which its accumulation sometimes induces. The cells may contain 
larger and smaller droplets of colloid material, or it may nearly or en- 
tirely replace the protoplasm, and accumulate to such an extent as to 
cause rupture and destruction of the cell. In this way, and by the 
atrophy of intercellular substance which its accumulation causes, cysts 



68 DEGENERATIVE CHANGES IN THE TISSUES. 

may be formed containing colloid material and cell detritus. Colloid 
degeneration is of frequent occurrence in certain tumors and in the 
thyroid gland, and occurs occasionally in other places. 

Hyaline Degeneration is the transformation of tissues into a trans- 
parent, glassy substance, much resembling amyloid in its morphological 
characters (Fig. 4) ; bat it does not give the micro-chemical reactions of 
amyloid, and appears under different conditions. Hyaline substance is 
quite resistant to the action of acids, and stains readily with acid fuch- 
sin and eosin. It occurs especially in the walls of the smaller blood- 
vessels in various parts of the body, in voluntary muscle fibres, and is 
said to sometimes involve interstitial tissue. It has been described as 
occurring in the brain, lymph glands, and ovaries; in the tubules of the 
kidney, in the Walls of aneurisms, in muscle fibres, in the lesions of 
diphtheritis, tuberculosis, and syphilis, in the hyaloid membrane and 
vessels of the eye, and elsewhere. It is sometimes called vitreous or 




Fig. 4.— Hyaline Degeneration of Capillary Blood-vessels. From a sarcoma of the optic 
nerve. 

fibrinous, and also waxy, degeneration. It seems to be, in some ways, 
allied to coagulation necrosis, but its exact significance and relations to 
other forms of degeneration, and the conditions of its occurrence, are 
not yet known. 

In Calcareous Degeneration there is a deposition, either in cells or 
in the intercellular substance, of larger and smaller granules composed 
chiefly of phosphate and carbonate of calcium. These particles, when 
abundant, give hardness, brittleness, and a whitish appearance to the af- 
fected tissue. Under the microscope, they appear dark by transmitted, 
white and glistening by reflected, light. The addition of strong acids 
causes their solution, usually with the formation of bubbles of carbonic 
acid gas, whose evolution may be observed under the microscope. Tis- 
sues may be nearly completely permeated with the salts, or the latter 
may be scattered in patches through them. Sometimes large, lamellated 
concretions are formed in tissues, usually at the seat of some old inflam- 



DEGENERATIVE CHANGES IN THE TISSUES. 69 

matory process. Calcification usually occurs in parts of tissues which 
are dead or are in a condition of reduced vitality, as a result of some 
antecedent morbid process, usually of an inflammatory nature. Among 
the most common and important examples of calcareous degenerations 
may be mentioned those which occur in the valves of the heart and walls 
of the blood-vessels. ■ 

Pigmentation. — The pigment which is present in the body under 
abnormal conditions may be formed in the body or may be introduced 
into it from without. It may be deposited in the cells or in the inter- 
cellular substance., and is sometimes visible to the naked eye and some- 
times not. The pigment occurring in the body may be in the form of 
yellow, brown, black, or reddish granules, or in crystalline form. In 
the majority of cases, the pigment is formed by the decomposition of 
haemoglobin from extravasated masses of red blood-cells. Parts which 
have been the seat of long- continued hyperemia may have a diffuse 
grayish appearance from the alterations of the haemoglobin in red blood- 
cells which have escaped from the vessels by diapedesis. Pigment may 
be formed in the blood-vessels in severe cases of malarial infection, and 
circulate in the blood. In another class of cases, various forms of cells 
seem to be actively concerned in elaborating pigment; this is exemplified 
in the true melanotic tumors, and the process has its physiological 
prototype in the formation of pigment in the choroid, skin, and some 
connective tissues. Pigmentation of tissue from the bile occurs under a 
variety of conditions, and may be the result of the deposition of granules 
or crystals. A diffuse staining also frequently occurs from the bile 
without the formation of solid particles. 

In many cases, the mode of formation of pigment is not at all under- 
stood. In tissues which are normally somewhat colored, the color may 
greatly deepen by a simple atrophy of the tissue without the new forma- 
tion of pigment, as in simple atrophy of the heart-muscle and in atro- 
phied fat. 

As examples of pigment introduced into the body from without, we 
may mention the deposition of minute particles of silver from the in- 
ternal use of silver nitrate; the coloring of the skin and lymph glands 
from tattooing; audi especially the pigmentation of the lungs and 
bronchial glands from the inhalation of coal and other dust, which is 
universally present under the conditions which modern civilization im- 
poses. 1 

1 For the literature on the subjects treated of in this chapter, see the extensive 
bibliography in Becklingfiauseri s "Handbuch der Allgemeinen Pathologie," which 
constitutes parts 2 and 3 of Billroth and Luecke's " Deutsche Chirurgie," 1883. 



PAEASITES. 



The scope of this work permits us to do little more than enumerate 
and give a very brief description of some of the more important forms of 
animal parasites found in man. Among the vegetable parasites, how- 
ever, the bacteria have assumed such an important place in the considera- 
tion of the etiology of certain diseases that they justly claim a somewhat 
extended notice. 

ANIMAL PARASITES. 

PROTOZOA. 

Among the unicellular organisms, several genera and species occur in 
the human body, but none are of great pathological significance. A spe- 
cies of amoeba has been found a few times, in Egypt and elsewhere, in 
large numbers in the intestinal contents in dysentery. Amoeba has also 
been found in the mouth. The so-called psorospermim — minute oval 




Fig. 5.— Cocoidium oviforme. From liver of rabbit. 

Showing phases in the development of the psorospermiae, which are seen separate within the 
capsule in C. After Braun. 

structures about .035 mm. long, with a thick capsule and coarsely 
granular contents — which are of very frequent occurrence in the liver 
of the rabbit, forming a part of the contents of yellowish, irregular- 
shaped cysts, have been found three or four times in the liver of man. 
The organism is more properly called Coccidium oviforme, while the 
spores which it forms are termed psorospermiae. 

Another, smaller form, occurring in the intestinal epithelium of dogs, 
cats, and rabbits, has been found in two cases in a similar situation in 
man. 

Among the infusoria we find in man representatives of several 



PARASITES. 



71 



genera. The more common of these are Cercomonas intestinalis, a 
pear-shaped, flagellate structure (Fig. 6) about 0.012 mm. long, making, 
when alive, rapid movements. It has been found in the evacuations of 
persons suffering from cholera, typhoid fever, and diarrhoea. 




Fig. 6.— Cercomonas intestinalis. After Braun. 

Trichomonas vaginalis has an oval or pear-shaped body, about 0.01 
mm. long, on which are a few cilia, and at the end two or three flagellse, 
somewhat longer than the body (Fig. 7). They are of very frequent 
occurrence in acid vaginal exudations in catarrhal vaginitis. The pos- 
sibility of mistaking the T. vaginalis for human spermatozoa should be 
borne in mind in medico-legal examinations, although to an observer 
familiar with either structure such a mistake could hardly occur. 




Fig. 7.— Trichomonas vaginalis. After Braun. 

Some forms of ciliated infusoria have been found in large numbers 
in the intestines in typhoid fever, particularly in the north of Europe. 
Most of the above-mentioned parasitic protozoa are apparently of little 
significance and simply accompany, not cause, the lesions with which 
they are occasionally associated. 



WORMS. 



Trematoda (Flukes). — These worms are small, flat, tongue-shaped 
or leaf-like creatures, with an intestine, and discoidal structures on the 
under surface, by means of which they attach themselves. There are 




Fig. 8.— Distoma hepaticum. About natural size. 



several genera and species found in man. The most common genus is 
Distoma. Of these, D. liepaticum is ol most frequent occurrence (Fig. 8). 



72 PARASITES. 

It is about 30 mm. long, and usually occurs in the gall-ducts and 
gall-bladder. The embryos are attached generally to water plants, from 
eating of which the infection is believed to occur. D. lanceolatum is 
more slender, pointed at the ends, 8 to 10 mm., long, and has been found 
a few times in the gall-bladder. D. sinense is a slender worm about 15 
mm. long, and has been found in the bile in considerable numbers, 
particularly in the Chinese. D. licematobium is a more nearly cylindrical 
worm ; the sexes are distinct; the male from 12 to 14 mm. long, the 
female 16 to 18 mm. long, and occurs especially in Egyptians, in the 
portal and other abdominal veins. . * 

Oestoda (Tape Worms). — These important worms consist, in the 
mature state, of more or less rectangular or elongated segments, each one 
of which represents a single individual, arranged in a linear series to form 
a colony, at one end of which, called the head, is a variously formed 
structure for the attachment of the colony to its host. The neck and 
head are called the scolex, while the segments are called proglottides. 
These worms have neither mouth nor alimentary canal. They are her- 
maphrodites, the sexes being united in the proglottides. The head and 
neck (scolex) may exist as an immature form in various tissues and organs 
where they are incysted, and are often called cysticercus. 

Tcenia solhim is of frequent occurrence in man. It may be several 
metres in length, and may be coiled up or stretched out in the small in- 
testines. Several worms may be in the gut at one time. The head, 
about the size of a pin's head (Fig. 9), has a projecting proboscis or ros- 
tellum, around which are arranged a double row of horny hooklets. 
Below these are four sucking discs at the sides of the head. The hook- 
lets of the anterior row are larger than those in the posterior row, and are 
from 0.16 to 0.18 mm. long. The proglottides, when fully developed, 
are from 10 to 12 mm. long, and from 5 to 6 mm. wide, but those nearest 
the head are much shorter and immature. The eggs of T. solium are 
ovoidal structures, about 0.03 mm. in diameter. The embryo of this 
worm is most commonly seen in the muscles of the pig as an incysted 
scolex, commonly called a "measle." It occasionally occurs in man in 
the muscles, brain, eye, etc., and is called cysticercus cellulosce. It is 
usually about the size of a pea, but may be as large as a pigeon's egg, 
and surrounded by a connective-tissue capsule. 

Infection with the worm occurs in the human subject from the in- 
gestion of insufficiently cooked "measly" pork, or, in the case of cysti- 
cercus cellulosse, from the ingestion of the eggs, which may, in a variety 
of ways in uncleanly persons, get into the food. 

Tcenia mediocanellata (T. sayinata Leuckart). — The head of this 
species is somewhat cuboidal, without either rostellum or hooklets, but 
with four sucking discs (Fig. 10). The segments are generally broader 
and shorter than in T. solium, and the worm is usually larger. In the 



PARASITES. 



73 



embryonal form the seolex occurs as the Cysticercus tmnicB medioca- 
nellatce in the form of small cysts in the muscles of cattle, from the eat- 
ing of which in the uncooked condition the infection occurs. This is the 
most common tape-worm in the United States. 

Tcenia ecliino coccus. — This worm in the mature condition forms a 
short, small colony inhabiting the intestine of the dog. The head is about 
0.3 mm. in diameter and has a double row of hooklets around the ros- 
tellum. The proglottides are three or four in number, the last being 
the larger. The entire colony is not more than 4 to 5 mm. in length. 
The significance of this parasite in human pathology depends upon the 



^ys^ 



•■: ■" ,,/ 



¥ 




Fig. 9. FlG . 10 

Fig. 9.— Head of Taenia solium, x about 40. 
Fig. 10. — Head and Proglottides of Tjenia medtocanellata 

A, Head, x about 15. 

B, Mature proglottid, showing generative apparatus. 

C, Head and fragments of immature proglottides, showing gradual tapering of the neck» 
Natural size. 

cysts, called hydatids, which it forms, in the immature or cysticercus 
stage, in various parts of the body. When the eggs of the mature worm 
get into the intestinal canal of man, they undergo partial development 
and find their way into the tissues and organs, most frequently into the 
liver. Here cysts are formed which become incapsulated by a connec- 
tive-tissue membrane produced by the inflammatory reaction of the 
organ. 

The cyst- wall of the parasite is formed of two layers — an outer, finely 



74 



PARASITES. 



lamellated layer called the cuticula (Fig. 11), and an inner, granular layer, 
containing muscle-fibres and blood-vessels, called the parenchymatous 
layer. Inside of the primary cyst, secondary cysts sometimes form, 
called daughter cysts, and within the latter tertiary cysts, called grand- 
daughter cysts, may develop. On the inner surface of the cysts, either 
primary, secondary, or tertiary, the scolices or heads of the immature 




Fig. 11.— Cuticula of Echinococcus Cyst, showing Lamellated Structure. 

worm are formed (Fig. 12). These develop in the walls of the pedi- 
culated vesicles called brood . capsules. The walls of these vesicles have 
a lamellated cuticula and a parenchymatous layer similar to those of the 
primary cysts. The scolices, of which there may be several in each brood 
capsule, are similar to the heads of the mature tape- worm. They are 
about 0.3 mm. in diameter, having a rostellum surrounded by a double 
row of hooklets and four sucking discs. At the posterior end of the 




Fig. 12. — Scolices of T^nia echinococcus, X 60. 
In one the rostellum is projecting, in the others it is withdrawn. 

scolex is a pedicle by which it is originally attached to the wall of the 
brood capsule. Little, lamellated concretions of lime salts are often pre- 
sent in the scolex. The anterior portion of the scolex, the rostellum, 
hooklets, and suckers, are often invaginated in the posterior portion. 
The scolices may be free inside of the brood capsules, or, owing to the 



PARASITES. 75 

rupture of the latter, they maybe free in the cavity of the primary cysts. 
They may die and degenerate, forming a granular mass in which the 
hooklets may be imbedded, or the hooklets may be free in the brood 
capsules or in the primary cysts. Sterile cysts are often found, that is, 
those in which neither brood capsules nor scolices are developed. 

The cysts contain, in addition to the scolices, a clear, gelatinous fluid. 
This fluid may become turbid by admixture with disintegrated scolices 
or fragments of the* parenchymatous layer, or it may contain fatty 
detritus, cholesterin crystals, and particles of lime salts. The fluid may 
be partially absorbed, leaving a thick, grumous material within the cysts, 
which may become calcified or converted into a stony mass. When the 
scolices are not found entire, the diagnosis may be made by the discovery 
of the separate hooklets (Fig. 13), or fragments of the characteristi- 
cally lamellated cyst-walls. The connective-tissue walls of the primary 
cysts may become fatty or cheesy or calcified. 

Sometimes the secondary vesicles project outward instead of inward, 
forming a series of cysts outside of the primary one. This variety of 




Fig. 13.— Hooklets from Scolex op Tjenia echinococcus. 

development is sometimes seen in man, but is more common in the do- 
mestic animals. It is called Ecldnococcus scohcijjariens or exogena. 

Another variety of echinococcus, called E. wultilocularis, is almost 
always found in the liver, and appears to be the result of incomplete 
and disturbed development of the embryos or cysts. It consists of 
a congeries of irregular, usually small cysts, surrounded by broad 
and narrow bands of connective tissue, and sometimes containing gela- 
tinous fluid and scolices or hooklets; but the latter structures are com- 
monly absent or difficult of detection. The whole is often surrounded 
by a dense connective-tissue capsule which may be calcified. The entire 
mass often presents an alveolar structure, and was formerly regarded as 
a tumor — alveolar cancer. The diagnosis may be established by the 
discovery of the hooklets or scolices, or fragments of the lamellated cu- 
ticula. 

There are four or five other species of taenia, occurring rarely in man. 

T. nana. — This species occurs in the form of small colonies about 
15 mm. in length. The rostellum is surrounded by a single row of 



76 PARASITES. 

hooklets. It has been seen once in large numbers by Bilharz in the 
duodenum of a child which died of meningitis in Cairo. 

T. flavopunctata, a species about which little is known, is reported 
twice in America as occurring in the intestine of young children. 

T. madagascariensis, also little known and rare, has been seen in two 
children in Madagascar. 

T. cuGumerina. — This species occurs in colonies about 20 cm. long. 
The head is very small and spheroidal, and has four rows of hooklets. 
It is frequent in the small intestines of dogs or cats. It occurs occasion- 
ally in man. Its scolex inhabits the dog louse, and infection may occur 
in man by the transference of the lice or the embryos of the parasite to 
the mouth, as the result of the filthy habit of kissing dogs and cats, or 
permitting the face to be licked by them. 

Bothrioceplialus latus. — This, the largest of the human tape-worms, 
has very broad, quadrangular proglottides. The head is ovoidal and 
about 2 mm. long and 1 mm. broad. It has no proper sucking discsand 
no hooklets; but by long grooves on either side of the head the animal 
attaches itself to its host. The neck is long and filiform. It occurs 




Fig. 14.— Ascaris lumbricoides. About half natural size. 
A, Male. B, Female. After Perls. 

most frequently in Europe, particularly in the northern provinces. The 
eggs undergo partial development in water, and are taken up by the pike 
and eel-pout, and perhaps by other fresh-water fish, from the ingestion 
of whose flesh in an imperfectly cooked condition the human infection 
occurs. Two other species of Bothriocephalus have been described as of 
rare occurrence in man : B. cordatus in Greenland and Iceland, and B. 
cristatus. 

Nematoda (Round Worms). — These worms are in general cylindrical, 
elongated, usually pointed at the ends, and sometimes filiform. The 
surface is sometimes smooth, sometimes irregularly beset with hairs and 
papillae, or possesses longitudinal elevated striae or transverse rings; but 
the body is not segmented. There is a mouth at the anterior portion, 
and a ventral anus near the posterior end. The intestine is straight. 
The sexes are in most forms distinct, the male being in general smaller 
than the female. 

Ascaris lumbricoides. — This is one of the most common of the human 
intestinal parasites, and is of particularly frequent occurrence in children. 
It is of a light brownish or reddish color. The female is from 30 to 40 
cm. long, and from 5 to 6 mm. thick. The male is somewhat more than 



PARASITES. 77 

half as large (Fig. 14). Both sexes are pointed at the ends, the posterior 
end of the male being curved into a spiued hook. The eggs, from 0.05 to 
0.06 mm. in diameter, are surrounded by an albuminous envelope, and 
are quite resistant to destructive agencies. The mode of development 
and life history of these parasites are not very well understood. Their 
usual seat in man is the small intestine, but they may wander into the 
stomach, and exceptionally get into the mouth, nose, bronchi, gall pas- 
sages, peritoneal cavity, etc. They may be single in the gut or present 
in great numbers. 

Two other species of ascaris have been found in man. A. maritima 
was found in the vomit of a child in Greenland, in an immature condi- 
tion. A. mystax, a tolerably common form in cats and dogs, has been 
found a few times in man. It is smaller than A. lumbricoides. 

Oxyuris vermicularis (Thread-worm or Pin-worm). — This species is 
very small; the female has a pointed tail, and is about 1 cm. long. The 
posterior end of the male, which is about 4 mm, long, is blunt, and after 



■h S 
Fig. 15.— Oxyuris vermicularis. 
A, Female. B, Male. 

death somewhat curled (Fig. 15). The eggs are produced in great num- 
bers, are oval, and about 0.052 mm. loug. This parasite is very common 
in children, and may be present in large numbers in the colon. They 
may, in the female, enter the vagina and uterus. This worm is only 
known to infest the human subject, and infection doubtless occurs by 
the ingestion of the eggs, which are widely distributed in a variety of 
ways on many objects, fruits, etc. 

Strongylus gigas. — This is a slender red worm, the female being 
sometimes 1 metre long and over 1 cm. in diameter. It has been found 
several times in the pelvis of the kidney in man. It is more common in 
the wolf, fox, horse, seal, and some other animals. Strongylus longeva- 
ginatus. — The female is about 2.5 cm. long, the male, as usual, shorter. 
It is of a yellowish-white color, and has been found once in the lung of a 
boy in Germany. 

Dochmiits duodenalis. — The female is from 1 to 2 cm. long, the male 
about 1 cm. long. The body of the male is dilated anteriorly and curved 



78 



PARASITES. 



backward. Its mouth is furnished with a chitinons capsule and chiti- 
nous claws and teeth. It isfound in" the small intestine of man in Italy, 
Switzerland, Egypt, and Brazil. The head is harrowed into the mucous 
membrane of the host, and the animal is nourished by the blood which 
it sucks out, and which is usually seen in its intestine. An ecchymosis 
is produced at the point of attachment, or even severe haemorrhage, and 
marked anaemia may be the result of the presence of large numbers of 
the parasites. 

Trichocephaliis dispar (Whip- worm). — The males and females are 
of nearly equal size, 4 to 5 cm. long. A little less than one-half of the 
body (the posterior portion) is about 1 mm. thick, and in the male is 
rolled into a flattened spiral, but in the female is but slightly bent. The 
anterior part of the body is very slender, and is imbedded in the mu- 
cous membrane of the host. The eggs are elongated, oval-shaped, about 




- [ nj. j'w- 






11 

Fig. lC— Trichina incysted in Muscle. 
In one capsule the worm is dead and its remains calcined 



mm 



0.05 mm. long and about one-half as wide, with a thick brown capsule. 
This parasite is very common in some countries; it dwells in the caecum 
in small or large numbers. It is usually of li ttle pathological significance, 
commonly producing no symptoms. Its developmental history is not. 
well known. 

Trichina spiralis. — The female of this most dangerous and common 
parasite is, in the mature condition, about 3 mm. long, the male from 1 
to 1.5 mm. long; they are filiform in shape and white in color. The 
young are born in the form of tiny worms about 0.01 mm. in length and 
somewhat similar to the adult in shape. Infection occurs in man from 
the ingestion of insufficiently cooked pork. The muscle of the diseased 
pig contains the embryos of the parasite in an incysted condition. In 
the stomach, the capsule of the worm is dissolved and the embryos are 
set free. They very rapidly mature, increasing in size, and the females 
give birth in the small intestine to very large numbers of young. It is 



PAEASITES. 79 

estimated that a single female may give birth to from 1,300 to 1,500 
young. These find their way through the mucous membrane and wall 
of the gut into various parts of the body. 

The exact course which they take in getting out of the gut is not 
fully established; probably they traverse the tissues in different ways. 
At any rate, they find their way to the voluntary striated muscle tissue, 
which they penetrate, and enter the muscle fibres. Here they cause a 
disintegration of the contractile substance, and coil themselves inside of 
the sarcolemma. In this situation they become incapsulated by mate- 
rial in part furnished by themselves, in part by means of the inflamma- 
tory reaction which their presence induces in the connective tissue of 
the muscle. The worms are surrounded inside the capsule by granular 
material (Fig. 16). The capsule after a time becomes partially calci- 
fied, and in this condition may be readily seen by the naked eye as a tiny 
white speck. In this incysted state they may remain inactive but living 
for an indefinite, often for a very loug time. Most frequently the cysts 
contain but one embryo, but they may contain from two to four. The 
embryo may die and its remains become calcified. 

The same course of events transpires when the muscle trichinae are 
eaten by the pig or a variety of other animals. 

The embryos in the muscle are killed by a temperature of 55° 0. 

The embryos may mature and a new generation be born within from 
five to eight days after the ingestion of the diseased meat. 

As the result of the presence of these parasites in the body, if the 
invasion be severe, acute catarrhal enteritis, with diarrhoea and vomit- 
ing, high fever, and severe pains, are apt to occur. (Edema of the face 
and of other parts of the body, broncho-pneumonia, and fatty degene- 
ration of the liver, may be found at the post-mortem examination of 
cases which have succumbed to the disease. The incapsulated embryos 
may be found in enormous numbers in various voluntary muscles of the 
body, but they are most apt to be found, when not very abundant, in 
the muscles of the neck and larynx, in the intercostals and the dia- 
phragm. They tend to collect towards the tendinous extremities of the 
muscles. Trichinae also occur in the rat, cat, mouse, and other animals. 1 

1 For the examination of muscles for the detection of the presence of the parasite, 
small pieces are snipped out with the scissors, and squeezed into a thin sheet between 
two slides, and examined with a low power. A considerable number of bits of muscle 
should be examined, particularly from the above-mentioned favorite situations, before 
excl uding them in a suspected case, because they are sometimes present in small num- 
bers. A thorough search is of especial importance in the examination of pork, since, 
owing to the enormous fertility of the parasites, even a moderate number may give 
rise to a severe infection. 

For the minute examination of the parasite, bits of muscle should be hardened in 
Miiller's fluid and alcohol, and decalcified if necessary, and, after imbedding in cel- 
loidin, thin sections cut and stained double with hematoxylin and eosin, and mounted 



80 PARASITES. 

Filaria medinensis (Guinea worm). — This is a thread-like worm; the 
female, which, is alone known, being sometimes as much as 80 cm. long 
and from 0.5 to 1.7 mm. thick. It is common in the East, and inhabits 
the subcutaneous connective tissue, in which it often gives rise to ab- 
scesses and ulcers. The embryos live for a time free in fresh water, and 
are then taken up by a species of fresh- water crustacean, in whose body 
they undergo further development, and by the ingestion of which the 
infection of the human subject occurs. 

Filaria. sanguinis hominis. — The embryo of this parasite, which in- 
habits the blood of men, especially in Brazil, Egypt, and some parts 
of the Orient, and occasionally occurs in this country, is about 
0.35 mm. long, rounded anteriorly, and pointed at the tail (Fig. 17). 
It has about the diameter of a red blood-cell. It occurs, sometimes in 
great numbers, in the blood during the night-time, being as a rule absent 
during the day. It may occur in the urine in connection with chyluria 
and hematuria. The mature female is from 8 to 10 cm. long, and has 
been found inhabiting the lymph vessels of man, particularly in the 




Fig. 17.— Filaria Sanguinis Hominis. 

From a case in the New York Hospital. The specimen was prepared and loaned to the writer 
by Dr. F. Ferguson. 

scrotum and lower extremities. Owing to the obstructions which it 
causes in the lymph circulation and to the local irritation which its pre- 
sence induces, it sometimes gives rise to'lymphangiectasis, oedema, ab- 
scesses, and perhaps elephantiasis. One of the embryonic stages of de- 
velopment is believed to transpire in the body of a species of nocturnal 
mosquito. Through the bodies of the dead mosquitoes, which are liable 
to fall into the drinking-water, it is believed that the spread of the 
parasite may occur. 

There are several other species of filaria occasionally found in man 
which it is not necessary to enumerate here. 



in balsam. Bits of muscle may be also teased, the embryos picked out with a needle, 
and the cysts either broken open under a lens with the needle, or squeezed under the 
cover-glass. The embryo worm thus set free may be mounted in a mixture of equal 
parts of glycerin and picric acid. The adult forms, which may be obtained by feed- 
ing rabbits with uncooked trichinous muscle, and examining after the proper interval, 
may be hardened in Muller's fluid, and mounted in a mixture of equal parts of picric 
acid and glycerin, or in the same mixture which has been lightly tinged with eosin. 






PARASITES. 



81 



RhaMonema strong yloides. — A small filiform worm from 1 to 2 mm. 
in length is found, often in enormous numbers, in the intestines, biliary 
and pancreatic ducts of man in Cochin China, giving rise to endemic 
chronic diarrhoea. It has been thought that there are at least two spe- 
cies, which have been described under the generic name Aguillula, but 
recent researches by Leuckart have led him to believe them to be dif- 
ferent developmental stages of the same form, for which he suggests the 
above name. 

ARTHROPODS. 

The scope of this work does not permit us to enter in detail into the 
subject of external parasites, which will be found described in treatises 
on diseases of the skin, or in the general works on parasites referred to 
below. But, owing to their frequent occurrence and practical importance, 
we may briefly describe two of the more common forms of arthropods, 
the " itch insect " and the " louse." 

The common "itch insect " — Sarcoptes hominis (Acarus scabiei) — 
is shaped somewhat like a turtle, with a chitinous covering, and presents 
the general appearance seen in Fig. 18. The female is about 0.45 mm. 
long; the male a little smaller. 





Fig. 18. Fig. 19. 

Fig. 18. -Sarcoptes hominis— the "itch insect.'' 1 Female; back view. After Fiirstenberg. 
Fig. 19.— PEurcoxus capitis— "head louse. 11 Male. After Braun. 



The parasite bores little tunnels in the skin in which the eggs are 
laid and the young hatched. After a few days these bore fresh channels 
in the skin. For their detection a bit of the superficial layer of the skin 
is snipped out with curved scissors, dehydrated and cleared up with oil 
of cloves, and examined under a low power, when the tunnels and the 
parasites, if present, will be readily visible. 

The head louse, Pediculus capitis, is from 1 to 2 mm. long, the 
female being slightly the larger. The general appearance of the insect 
is seen in Fig. 19. 
6 



82 PARASITES. 

MODES OF STUDY AND PREPARATION OF THE ANIMAL PARASITES. 

The protozoa may be studied in the living condition in one-half-per- 
cent solution of sodium chloride. They may be killed and preserved by 
allowing a drop of one-per-cent osmic acid to run under the cover-glass, 
and replacing this after a few hours by glycerin lightly tinged with 
eosin. The smaller and embryonic forms of the various kinds of para- 
sitic worms may be hardened, best under the cover-glass, with Muller's 
fluid or osmic acid, and these may be, when the hardening is completed, 
replaced by dilute, and this by strong alcohol, and the latter finally 
replaced by eosin-glycerin, in which the specimens are permanently pre- 
served; or they may be stained lightly by tinging the alcohol with eosin, 
and then cleared up by oil of cloves, and finally mounted in balsam. 

It is necessary; however, for detailed study of the larger parasites, 
to make thin longitudinal and transverse sections from different parts 
of the body. This can be readily done, even in very small forms, 
by imbedding the animal — after careful hardening in osmic acid or in 
Muller's fluid, and afterwards in alcohol — in celloidin, and using the 
microtome. The sections may be stained double with hematoxylin and 
eosin, and mounted in balsam. 

The general arrangement of the generative organs in the proglot- 
tides of tape worms may be well seen by staining in eosin or eosin-gly- 
cerin after moderate hardening in dilute alcohol, and then squeezing 
the segment between two glass slides. The itch insect and louse may 
be soaked for a few hours in turpentine and mounted in balsam. 1 

1 Bibliography. — Especially to be recommended for detailed descriptions of human 
parasites, together with practical suggestions for their study, is the small work of 
Braun, il Die thierischen Parasiten des Menschen," 1883, which contains also the more 
important bibliography. 

The more extended classical works of Cobbold, "Entozoa of Men and Animals," 
1,879, and Kuclienmeister and Ziirn, "Die Parasiten des Menschen," 2d ed , and the 
work of Leuckart, "Die Menschlichen Parasiten," should be consulted, and contain 
valuable bibliography. Various forms of external parasites of men and animals are 
fully described and illustrated in the work of Megnin, * ' Les Parasites et les Maladies 
parasitaires chez l'homme," etc., 1880. The plates of Stein, illustrating the Cestoda, 
1882, are carefully executed. In the " Report on Trichina? and Trichinosis," in 1880, 
by Glazier, Surgeon in the Marine Hospital Service, will be found an illustrated 
account of the natural history of this parasite, history of the disease, etc., and a sec- 
tion on its occurrence in the United States. 



t t <t 5? 



VEGETABLE PARASITES. 



PARASITIC FUNGI. 



These lowly vegetable organisms, which are of not infrequent occur- 
rence on and in the human body, both in health and disease, embrace 
the structures commonly known as moulds and yeasts. Of these, the 
moulds are of the greatest importance, and these present varying 
degrees of significance. The scope of this work does not permit us to 
describe either the natural history of the group or the different forms. 
For this we refer to works on skin disease and on vegetable parasites. 

We may simply mention as the more common and important the 
Achorion Sch'onleinii, or favus fungus; the Trichophyton tonsurans, or 
ringworm fungus; the Microsporon furfur, or the fungus of pityriasis 
versicolor. A form of Aspergillus is of occasional occurrence in the 
external meatus of the ear and on the membrana tympani. The pecu- 
liar white pellicle often seen on the mucous membrane of the mouth and 
pharynx, sometimes in adults who are the victims of exhausting dis- 
eases, but more often in young children {thrush), is associated with the 
fungus Oidium albicans (Saccharomyces albicans). 

Actinomyces (ray fungus). — This fungus grows in radiate masses, 
especially in the jaws of cattle, but is of occasional occurrence in man. 
The disease which it causes is called actinomycosis. The fungous mass 
may form a large tumor in the jaw, by its own growth and by the forma- 
tion of granulation tissue, which is apt to slough and spread so that 
not only may the tissues of the tongue, pharynx, larynx, etc., be involved, 
but nodules of similar character may form in the gastro-intestinal canal, 
lungs, skin, etc. These nodules were formerly considered to be some 
form of sarcoma. The fungus forms little yellow masses as large as a 
millet seed or smaller, which are scattered through the new-formed 
granulation tissue or mingled with the pus, giving the growths a very 
characteristic appearance. It is the peculiar radiate grouping of the 
filaments of the growth (Fig. 20) which gave rise to the name '" ray 
fungus/' The disease is propagated from one animal to another by 



84 VEGETABLE PARASITES. 

inoculation or by contact of the growth with a wound or an abrasion of 
the mucous membrane. 1 

For convenience, the actinomyces is here mentioned in connection 
with the fungi, but its life history and affinities are too little known as 
yet to enable us definitely to classify it. 

The tissue containing actinomyces may be teased in a fresh state 






i^^M&^mmz 



Wm% 










Fig. 20.— Actenomyces bovis, showing one of the yellowish masses of the parasite separated 
from the surrounding tissue. 

and stained in an alcoholic solution of eosin. Sections of the diseased 
tissue may be stained double, first for an hour with orseille and then 
with gentian violet 

BACTERIA. 

Morphology and Physiology. — Bacteria are minute vegetable organ- 
isms of the lowest and simplest form allied to the algae. They are 
widely distributed in the air, water, and surface soil, and are particularly 
abundant among the habitations of men, or wherever animal and vege- 
table substances are undergoing decay. Putrefaction and putrefactive 
products are always dependent upon their presence and activity. 

The bacteria play a very important role in nature in virtue of their 
power of feeding upon and pulling to pieces dead organic materials. A 
small part of the new chemical compounds which are thus formed are 
used by the bacteria themselves for the purposes of their own nutrition 
and growth, while the rest are set free to serve, sooner or later, as food for 
other forms of plants or animals. Some of the chemical compounds set 
free by the growing bacteria are bad-smelling or aromatic gases ; some 
are inert and harmless substances; some are powerful poisons, and may, 
when they have accumulated in the fluids where they grow, destroy the 
bacteria which have produced them. 

1 For general consideration of the fungi and their relations to disease, consult 
Flugge, " Mikro-organismen," 1886. 



VEGETABLE PARASITES. 85 

Bacteria of one kind or another are invariably present in greater or 
less numbers in the mouth, nose, lungs, and gastro-intestinal canal of 
men and animals. The largest of them are too small to be seen with the 
naked eye, and the smallest require for their recognition the most perfect 
and powerful of our microscopic aids. They have various shapes: 
spheroidal, rod-like, filiform, or spiral. They are simple cells, multi- 
plying, when the conditions are favorable, with extraordinary rapidity, 
by transverse division, or by the formation of spores which develop into 
the adult forms. They are formed of a membrane inclosing the proto- 
plasm, which may appear homogeneous or granular. 

They lie sometimes singly, sometimes in pairs or chains, and some- 
times in masses imbedded in a transparent gelatinous substance, and are 
then called zobgloea colonies. Some are capable of performing rapid 
movements, others not, and the same form may be at one time mobile 
and at another immobile. Some of them have a cilium at the ends by 
means of whose vibrations they may perform active progressive move- 
ments. Some are surrounded by a homogeneous envelope called a 
capsule. 

They require for their nourishment nitrogen and the hydrocarbons; 
oxygen is necessary for the proliferation and activities of some forms, 
and for others not. 

They are active only in the presence of moisture, but when this and 
other conditions favoring their activities fail they do not necessarily die, 
but some forms may remain, either as spores or as fully developed 
organisms, for long periods wholly dry and inert, but capable of resuming 
their activity whenever they are again restored to favorable conditions. 

Some are and some are not very sensitive to changes of temperature. 
At a temperature below 4- 5° C. they are incapable of activity or pro- 
liferation, but some forms are not killed by a temperature of —111° 0. 
As the temperature is raised, their activities increase up to a certain point. 
It may be said in general that they are most active at about the tempera- 
ture of the body, although species differ considerably in this respect. 
In fluids, many bacteria are killed by a temperature of 80° C, and all are 
killed by a temperature of 100° 0. (the boiling point of water) if this 
be long enough continued. When dry, they resist much higher tempera- 
tures than when moist. The spores are, as a rule, more resistant to high 
temperatures than the bacteria themselves; some having been exposed, 
dry, to a temperature of 140° C. without destruction of life. Fluids 
containing the spores of bacteria which resist very high temperatures 
may be sterilized by boiling for a short time, then being allowed to stand 
at ordinary temperatures for several hours, and then again boiling; this 
process being repeated several times. In this way, although the spores 
themselves are not killed by the heat, the bacteria into which they 



86 VEGETABLE PABASITES. 

develop during the intervals are killed, so that finally the medium is 
entirely freed from both living spores and adult bacteria. 

Certain disinfecting agents, when brought into contact with bacteria, 
are capable of greatly reducing their activities, or destroying them al- 
together; but different forms differ greatly in their power of resisting 
the action of these agents. The spores of certain bacteria are exceed- 
ingly resistant, much more so than the bacteria themselves, to the action 
of disinfecting agents. Among these disinfectants may be mentioned 
sulphurous acid, bromine, creolin, carbolic acid, and especially solutions 
of corrosive sublimate, which is very inimical to the life of most bacteria 
and their spores, even in extremely dilute solutions. 




Fig. 21.— Drawing of three typical Forms of Bacteria illustrating the Three Classes. 
Stained with fuchsin. 

Classification of Bacteria — The systematic study of these organisms 
by exact and reliable methods is of such recent date, they are so small 
and difficult to examine completely, and so much uncertainty still exists 
about the character and life history of many known forms, that a satis- 
factory and scientific classification of them is not yet possible. For the 
sake of convenience, however, we group the various known species ac- 
cording to their shape : 

I. Spheroidal bacteria. 

II. Rod-shaped or filiform bacteria. 

III. Spiral-shaped bacteria.* 

This classification or grouping of the bacteria is temporary and pro- 
visional, and as our knowledge increases will, no doubt, be essentially 

1 In addition to these, there are a few forms which present such variable shapes in 
different phases of their growth that they form a rather indefinite class by themselves. 

When the bacteria are growing under unfavorable conditions, or when they are old 
or dead, they may assume various distorted, bizarre shapes, which are called involution 
forms. 



VEGETABLE PARASITES. 87 

modified or altogether replaced ; but it is at present almost indispensable 
for purposes of study. 

I. SPHEROIDAL BACTERIA. 

The most common and important genus of this group of bacteria is 
Micrococcus, of which there are many species. Some of these are 
capable of producing coloring materials of various kinds in the 
nutrient media; others induce different forms of fermentation; still 
others occurring in the body in connection with various diseases are 
called pathogenic micrococci. The cells of most of the species of mi- 
crococci are very small, having, for the most part, a diameter of less than 
1 /i (0.001 mm.); but some forms are considerably larger. They occur 
either singly or joined together in pairs— diplococcus; in longer or 
shorter beaded chains — streptococci; or in zooglcea masses (Fig. 22). 
They are believed never to exhibit spontaneous movements, although 
liable to show the Brownian movement. The species differ from one 



v *♦ 



'i 



<v 



Fig. 22.— Spheroidal Bacteria (cents Micrococcus). 

1. Micrococcus from ulcerative endocarditis, a, single; 6, zooglcea. 

2. Micrococci cultivated from laboratory dust, a, in pairs (diplococcus form) ; 6, in tetrads 
M. tetragenous; c, in chains (streptococcus form). Stained with fuchsin. 



another in size, sometimes slightly in shape, in mode of grouping, in 
refractile power, and in their physiological activities. 

Among the color-producing micrococci may be mentioned the Micro- 
coccus luteus, which is common in the dust of the air, and, when growing 
in masses, forms yellow droplets on the surface of boiled potatoes or other 
nutrient media. 

The Micrococcus urece, which frequently occurs in urine, induces 
ammoniacal fermentation. Other species are found in fermenting wine 
and in a great variety of putrefying substances. 

The so-called pathogenic micrococci belong, as a rule, among the 
minuter forms, and morphological distinctions between the species are as 
yet, for the most part, wanting. 

Micrococci have been found at the seat of lesion or in various parts 
of the body in diphtheria, scarlet fever, erysipelas, ulcerative endocardi- 
tis, cerebro-spinakmenmgitis; pneumonia, rosted-rriyttitis, &ii&per%o'§titisj 



88 VEGETABLE PARASITES. 

pycemia, puerperal fever, gonorrhoea, and in connection with various 
phases of suppurative inflammation. 

Their occurrence and significance will be considered in the descrip- 
tions of the lesions of these diseases in the section of this book devoted 
to Special Pathology. 

Micrococci have been described as occurring in connection with a 
large number of other diseases, but without proof of their causative rela- 
tion to them. 

Another genus of sphero-bacteria is Sarcina, which embraces- several 
species. Among these is the 8. ventriculi, consisting of large cells 
usually grouped in clusters of four to sixteen. They are found in the 
stomach, both in health and disease, but are not proven to stand in a 
causative relation to the diseased conditions in which they occur. 

II. ROD-SHAPED OR FILIFORM BACTERIA. 

The most common and important genus in this group is called 



*v 



* / 

I 2 

Fig. 23. —Bacilli in Pairs 



1 was formerly called Bacterium termo, and 2 B. lineola. 

Bacillus. Some of the bacilli are short, and are apt to be grouped in 
pairs (see Fig. 23). 

Some are long and may form chains or threads (see Fig. 24) ; some 
are slightly curved, and when joined together end to end, as is apt to 
occur in their growth, they form spirals (Fig 2o). 







Fig. 24. Fig. 25. 

Fig. 24.— Bacilli arranged End to End, forming Chains. 

Cultivated from laboratory air. 

Fig. 25.— Curved Bacilli forming Spiral Chains. 
Spirillum tyrogenum. 

Some of the bacilli are immobile; others are capable of performing 
the most varied movements when suspended in fluids. Many of the 
bacilli are concerned in the ordinary processes of decay which we call 



VEGETABLE PARASITES. 89 

putrefaction, and are entirely harmless when introduced into the human 
or animal body. Many produce brilliant colors, red, yellow, green, etc., 
when growing in large masses. 

Certain bacilli are capable, when they gain access to the body, of in- 
ducing serious disease, and even death — pathogenic bacilli. Thus malig- 
nant pustule, tuberculosis, typhoid fever, leprosy, glanders, Asiatic 
cholera, have been proven to be caused by different species of bacilli, 
which will be considered later in this book under their appropriate head- 
ings. 

Bacilli of septicemia of mice. — Dr. Koch has described small bacilli 
— 0.8 to 1 pi long — occurring sometimes in pairs, sometimes in chains, 
which are found as spores or as developed bacteria in a great variety of 
putrefying fluids. They may be readily cultivated on gelatin, and the 
inoculation of the purified organisms or of the putrefying fluids into 




Fig. 26.— Schematic drawing of Bacilli (B, megateriom) containing Spores, . 

house mice produces symptoms characteristic of septicaemia. The bacilli 
may be found in great numbers in the leucocytes, in the subcutaneous 
tissue about the seat of inoculation, and very generally in the blood- 
vessels. The animals may die, or, if they survive, exhibit a marked im- 
munity from the characteristic effects of subsequent inoculations. Field 
mice are not affected by inoculation with these bacilli, and rabbits usu- 
ally but slightly. 

Bacilli of malignant oedema of mice, guinea-pigs, and rabbits. — These 
are from 3 to 3.5 jjl long, rounded at the ends. They frequently occur 
in pairs, and may exhibit spontaneous movements. They occur in culti- 
vated soil, in hay, putrefying fluids, and elsewhere. When introduced 
into the subcutaneous tissue of the above-named animals, they proliferate 
and produce a wide-spread oedema about the seat of inoculation. In the 
clear reddish, (Edematous fluid multitudes of the bacilli may be found, 
7 



90 VEGETABLE PARASITES. 

After death they may be found in the blood, in the juices of internal 
organs, or upon serous surfaces. It is very difficult to cultivate them 
outside of the body. A large number of other bacilli are known which 
cause disease when inoculated into animals. 

Leptothrix. — There exist under almost all conditions in the mouth 
and about the junction of the teeth and gums, single or in larger or 
smaller masses, long, slender, filiform bacilli, usually without transverse 
divisions, which have received the general name Leptothrix buccalis. 
There are some reasons for supposing that they may be concerned in 
caries of the teeth, in connection with which they are often found. But 
beyond this fairly well-founded conjecture, we have no reason to suspect 
them to be of any pathogenic significance. They are frequently entan- 
gled among scattered or larger and smaller masses of micrococci (Fig. 
27). Leptothrix is a general name only, and we do not know whether 




Fig. 27.— Leptothrix buccalis with Micrococcus Colonies. 
From the mouth of a healthy person. 

it represents a single genus or species, or whether it is made up of unde- 
veloped forms of some varieties of bacillus. 



III. SPIRAL-SHAPED BACTERIA. 

The spirals of these cells may be close or open, few in number or 
numerous; some of them are ciliated at the ends. One of the common 
genera of these bacteria is Spirillum. S. rugula occurs in swamp 
water, on the surfaces of the teeth, and in fasces. It is thick, has open 
spirals, and occurs in chains or interlacing masses. Other species, 
among which may be mentioned 8, serpens (Fig. 28), occur in stagnant 
water and in putrefying fluids. 

Another important genus of spiro-bacteria is Spirochete, whose cells 
are in general larger and more flexible than those of spirillum, with more 
closely set spirals. 

Spirochete denticola is found in the mucous membrane of the mouth 
and on the teeth mixed with leptothrix, and also in carious teeth. It is 
usually about 10 to 20 yw long, and pointed at the ends (Fig. 29). S. 
plicatilis is about 110 to 225 yu long, very slender, with many spirals, and 






VEGETABLE PARASITES. 91 

blunt ends. It moves with great rapidity, and is frequently found in 
summer in swamp water and in eave-troughs. 

One of the more important species of this group is that causing 
Relapsing Fever, under which heading it will be described. 

It should always be borne in mind, in examining tissues taken from 
the dead body, that various forms of bacteria commence to proliferate in 
the fluids and tissues very soon after death, and may develop in extra- 
ordinary numbers in a very short time. 

The bacteria are often divided into two great groups depending upon 
the conditions under which they live. Those which nourish themselves 
on dead organic material are called saprophytes or saprophytic bacteria ; 
those which feed upon living organisms, parasites or parasitic bac- 
teria. 

While some of the parasitic bacteria are always parasitic {obligatory 
parasites), there are others which are only occasionally parasitic; these 
are called facultative parasites. There are others, furthermore, which 





Fig. 28. Fig. 29. 

Fig. 28.— Spirillum serpens. 
From putrefying hay infusion. 

Fig. 29.— Spirochete denticola. 
From mouth of healthy person. 

usually are parasitic, but occasionally live as saprophytes; these are 
facultative saprophytes. 

This classification is by no means an exact one, but it serves a useful 
purpose in indicating in a general way the favorite life conditions of 
different forms of bacteria. 

The Relations of Bacteria to Disease. — Bacteria of various forms may 
occur on the surface of the skin and mucous membranes, and in the 
lungs, exerting no apparent influence whatever, so far as we can judge 
by morphological appearances, upon the surrounding parts. They may 
occur on the surface of wounds, ulcers, etc., without the production 
of any evident changes; they sometimes lie within cells which appear 
otherwise perfectly normal. On the other hand, the cells and tissues in 
their vicinity may show very marked alterations, which are presumably 
due to their influence. The cells may be swollen, their nuclei may 
break down or disappear, and the protoplasm may be converted into a 
*ass of shining or coarsely granular particles, or may completely disin- 
te "ate. The intercellular substance near the bacteria may also soften 



92 



VEGETABLE PARASITES. 



and disintegrate. In a word, the tissue in their immediate vicinity is 
often found in a condition of necrosis of one kind or another. The 
walls of blood-vessels near which they lie may die, and the blood which 
they carry may form thrombi. The bacteria may themselves enter the 
vessels and proliferate in the blood; they may be swept away as emboli 
to remote parts of the body (Fig. 30), and establish new foci of bacterial 
proliferation and tissue necrosis. Some forms, instead of causiDg the 
immediate death of the tissue, appear to incite inflammatory changes 
about themselves (Fig. 31). These may be simple, and similar to those 
produced by the presence of any irritating foreign body; or it would 
seem that the bacteria may determine, in some way as yet unknown to 
us, very peculiar and characteristic inflammatory changes, which may 




Fig. 30.— Bacterial, Embolus in the Blood 
Malignant Ulcerative Endocarditis. 



VESSELS OP THE GLOMERULUS OF THE KlDNEY IN 



result in the formation of new tissues of various kinds. Some forms of 
bacteria find in the blood, others in the lymph spaces and vessels, the 
conditions most favorable for their proliferation. 

As the bacteria grow in the tissues or fluids of the body, they form 
and set free various kinds of chemical compounds. These are called 
ptomaines; and some of these ptomaines are very poisonous indeed. It 
seems at present highly probable that a large proportion of the deleteri- 
ous effects which pathogenic bacteria may cause as they grow in the 
body are due to the ptomaines which they elaborate and set free. 

It will be seen, from what has now been said of the bacteria, that in 
different parts of the system in health, and in a large number of diseased 



VEGETABLE PARASITES. 



93 



conditions, various forms of bacteria occur; but it is quite evident that 
the significance which we must attach to their mere presence varies 
greatly. In a large number of cases, especially when on parts exposed to 
the air or in the gastro-intestinal canal, they are evidently of no more 
importance than so much inorganic dust. When, however, special forms 
of bacteria are found to occur uniformly in connection with well-defined 
diseases, or in their lesions, the conjecture is certainly justified that they 
may have something to do with their production. Yet in all such cases 
we have to consider the possibility that it is the diseased state or the 
character of the lesion, produced perhaps by other causes, which affords 







- - - . 






m 











^ 



l^«^S3WWSSiB» 



Fig. 31.— Colonies of Micrococci in a Blood-vessel op the Kidney causing a small 

From a case of pyasmia. 
Around the dilated and partially necrotic blood-vessel in which the bacteria lie is an area of 
necrotic tissue and small celled infiltration or zone of pus. 



conditions suitable for bacterial growth, and that they may consequently 
occur in considerable numbers; while in the absence of these conditions 
they would be unable to develop. Even the constant occurrence in the 
body, in certain diseases, of bacteria which evidently produce well- 
marked local effects, either inflammatory or degenerative, does not abso- 
lutely prove their causative relation to the disease, although it renders it 
to a certain degree probable. 



94 VEGETABLE PARASITES. 

In order to absolutely prove the bacterial origin of an infections dis- 
ease, we must not only be able to demonstrate the constant presence in 
the body at some time of a special form of bacteria, bnt we mast obtain 
them in an absolutely pure condition, unmixed with any other living 
thing, or with any chemical substance not belonging to them, and, by 
the introduction of the purified organisms into a healthy animal, be able 
to produce the disease in some definite form. When all this is done, 
and not before, can we assert with absolute certainty the causative rela- 
tion between a given form of bacteria and any special infectious disease. 
But the fulfilment of these strict requirements is very difficult in many 
cases, and in some, apparently, almost if not quite impossible; for we must 
remember, in the first place, that the lower animals, upon which alone, 
for the most part, inoculation experiments are practicable, are appar- 
ently not subject to certain important diseases of men; and second, that 
they present among themselves the most marked differences in the de- 
gree and manner in which they are affected by the inoculation of patho- 
genic bacteria. Desirable as is the complete fulfilment of the above 
requirements in every case, it must be admitted that a reasonable cer- 
tainty regarding the bacterial origin of a given disease may be arrived at 
without positive results from the inoculation of the bacteria associated 
with its lesions. 

The discussion of the probabilities of the bacterial origin of certain 
classes of disease, and the long series of phenomena exhibited by them, 
which the bacterial theory very satisfactorily explains, does not fall 
within the scope of this book. 

The complete demonstration which certainty requires has as yet been 
furnished in but a very small number of cases. In a considerable number 
of other cases, although the complete cycle of proof has not yet been 
established, enough has been done in the way of study and experimenta- 
tion to render it altogether probable that certain forms of bacteria are 
the cause of the diseases. 

Conditions Influencing the Occurrence of Bacterial Diseases. — It has 
been learned, as the result of a great deal of observation and experi- 
ment, that, although certain diseases are invariably caused by the pre- 
sence and growth in the body of particular species of bacteria, and 
never occur without them, still there are various other accessory factors 
which have a very important bearing upon the inception and course of 
the diseases. Thus, while the presence in the body of a particular 
species of bacteria is the most significant and fundamental of the de- 
termining agencies in the bacterial diseases, the numbers in which 
they are present — i.e., the size of dose — and the varying virulence which 
the same species under different conditions possesses, as well as the vary- 
ing capacity of resistance to the incursions of the germs which the body 



VEGETABLE PARASITES. 95 

cells at different times and under differing conditions exhibit, are all 
factors of the greatest moment. 

It should be always borne in mind that the human body is a great 
aggregate of groups of co-ordinated cells which, under normal conditions, 
all act in harmony for the maintenance of the life and functions of the 
individual. The cells and cell communities in health not only do this, 
but they have the power of resisting and to a certain extent overcoming 
the various deleterious agencies to which the body is more or less con- 
stantly liable. 

What we call hereditary or acquired predisposition to a bacterial 
disease, such as tuberculosis, for example, is simply a lack of the usual 
capacity of the cells of the body — whether through a structural or phy- 
siological fault we do not yet know — to cope with the destructive ten- 
dencies of the living bacteria when once they gain a foothold in the 
body. 

We thus see that, in studying the conditions under which bacterial 
diseases occur, the work is by no means complete when we have demon- 
strated the bacterial species which causes the disease, but that then the 
more obscure determining and influencing agencies must be worked 
out in each particular case. 

Phagocytes. — It is well known that the introduction into the body 
even of extremely virulent species of bacteria does not always cause dis- 
ease. It is furthermore established that when recovery from a bacterial 
disease occurs, the germs after a time disappear from the body. These 
well-known facts show either that the body possesses the power of 
directly destroying certain bacteria, or of furnishing conditions which 
are so unfavorable for their life that they die. 

It is believed by many that certain cells of the body are capable of 
taking up bacteria, which get into the tissues, into their protoplasm, and 
there destroying and perhaps digesting them, and that thus the destruc- 
tion of bacteria in the body may be brought about. 

Others believe that certain of the body cells, the leucocytes, for ex- 
ample, which are often found gathered about masses of bacteria in the 
body, cut off the supply of oxygen or nutriment from the germs and thus 
cause their destruction. 

The cells which take up into their bodies the bacteria, as well as other 
foreign bodies, are called Phagocytes. This assumed mode of destruc- 
tion of bacteria forms a most suggestive and fascinating hypothesis, but 
its significance and importance are not yet very fully demonstrated. 

The reasons for believing that certain well-known and important dis- 
eases are caused by bacteria, as well as a description of the particular 
organisms concerned, will be found in that part of this book which treats 



yb VEGETABLE PARASITES. 

in detail of the lesions of various parts of the body or of the lesions of 
the general diseases. 

METHODS OF STUDYING BACTERIA. 

The simplest mode of studying bacteria is to examine them either in 
the fluids in which they lie, or in thin sections of the tissues mounted 
in one-half-per-cent salt solution, and for the study of many of the phe- 
nomena of life this method is important. The tissue and other ele- 
ments, however, with which they are often associated, greatly interfere 
with the study of the bacteria, and many forms are so small as to be 
scarcely recognizable in the natural condition. 

By far the most important aid in the morphological study of the bac- 
teria is derived from the use of staining* agents. Most of the bacteria 
are stained more or less readily by one or more of the aniline dyes. The 
ease with which they are colored varies considerably in different species 
and with the different dyes. The tissue elements, and a variety of other 
materials with which the bacteria may be associated, also stain more or 
less readily at the same time; but most of these part with their color 
more readily than do the bacteria, on being treated with alcohol or 
dilute acids. We are thus enabled to obtain a differentiation in color 
between bacteria and other structures. The bacteria, moreover, differ 
among themselves in respect to the tenacity with which they hold their 
stain in the presence of decolorizing agents; and upon this fact is based 
one of the important methods of distinguishing between different 
species. 

Among the aniline dyes more commonly employed for bacteria stain- 
ing may be mentioned fuchsin, gentian violet, methylene blue, and Bis- 
mark brown. Of these, the fuchsin and gentian violet are the best for 
ordinary purposes. 

A. saturated alcoholic solution of these dyes should be kept in a 
tightly stoppered bottle, and from this the more dilute solutions re- 
quired for staining may be prepared. For ordinary purposes, one part 
of the alcoholic solution of fuchsin or gentian violet, added to twenty 
parts of water, will give a staining solution of suitable strength. This 
should be prepared in small quantities as required, since it does not keep 
well, and a granular precipitate is apt to form in a few days. 

Special stains and modes ol staining, such as are necessary for some 
forms of bacteria, such as the tubercle and typhoid bacillus, will be de- 
scribed under the appropriate headings. We are speaking here only of 
the general methods. 

To Stain Bacteria in Fluids. — A small drop of the fluid is placed on 
a cover-glass, spread a little with a needle, and allowed to dry by evapo- 
ration in the air or by gentle heating high over a flame. The cover- 
glass is now held with the forceps, and — specimen side up — passed mode- 



VEGETABLE PARASITES. 97 

rately rapidly three times through the flame of an alcohol lamp or a 
Bunsen burner. The material on the cover should not be burned. This 
heating not only fixes the contents of the fluid firmly on to the glass, so 
that it will not easily soak off, but it renders insoluble any albuminous 
materials which may be mixed with the bacteria, and which might other- 
wise interfere with subsequent examinations, by forming granular pre- 
cipitates. 

A drop of the aqueous staining fluid is now put on to the dried speci- 
men on the cover-glass, and if this be held in the forceps and tilted 
slightly up and down a few times, so as to bring fresh portions of the 
staining fluid into contact with the bacteria, the staining will usually 
be completed in two or three minutes. The stain is now washed off 
with a jet of water from the wash-bottle, and the specimen is either 
mounted directly in a drop of water for temporary study, or the washing- 
water is drained off, and after drying in the air is mounted directly in 
balsam. 

It is well to use balsam which has been softened, when this is neces- 
sary, with oil of cedar or xylol, since chloroform is apt to decolorize the 
bacteria. 

If the bacteria which are to be stained are in solid masses, as is apt to 
be the case in pure cultures on solid media (see page 99), a small drop 
of distilled water should be first put on the middle of the cover-glass, 
and a very minute quantity of the bacteria mass rubbed into it with a 
needle, and then dried and stained as before. 

To Stain Bacteria in Tissues. — The tissues should be well hardened 
in alcohol. Thin sections are placed in the above-described coloring solu- 
tions, where they may remain from one to ten hours. Gentle warming 
(40° to 50° C.) will hasten the staining. The entire tissue as well as the 
bacteria is in this way deeply colored. The sections are rinsed with 
distilled water and then placed in alcohol. This, with varying degrees 
of rapidity with different stains and tissues, gradually extracts the color 
from the tissue, most slowly from the nuclei. The time required and the 
exact degree of decolorization to be sought for must be learned by experi- 
ence in different cases. Sometimes five, sometimes thirty minutes are 
required. It is often necessary, and the decolorizing of the tissue is 
thereby hastened, to add a few drops of acetic acid to the alcohol. 
When acetic acid is used, it should be finally thoroughly washed out by 
alcohol. The specimens are now cleared up by oil of cloves and 
mounted in balsam. Oil of cloves removes the color from some forms 
of bacteria, and in this case xylol or oil of bergamot should be substi- 
tuted for it. In specimens prepared in the above way, the nuclei of cells 
usually retain to some extent a color similar to that of the bacteria, but 
their size and shape serve for the differentiation. 

A much more generally useful method of staining bacteria in thetis- 
8 



98 VEGETABLE PARASITES. 

sues than that just given, although not in all cases applicable, is that 
known as Gram's method. The tissues from which the sections are made 
should have been hardened and preserved in alcohol. The sections are 
stained for from two to four minutes in aniline-gentian-violet solution. 
This is prepared as follows: 5 c.c. aniline oil are added to 100 c.c. distilled 
water; this mixture is well shaken, and the excess of aniline oil is fil- 
tered off through a moistened paper filter. To the clear filtrate saturated 
alcoholic solution of gentian violet is added until the fluid becomes 
opalescent (about 1 part of the dye to 10 of the water will usually be 
enough). A small quantity only of this fluid should be prepared at once, 
as it does not keep very well. 

From the staining solution the sections are transferred directly to a 
solution of iodine in potassium iodide and water (I 1.0 — KI 2.0 — H 2 
300.0). In this they remain from one to three minutes, a precipitate 
forming in the solution and the sections becoming of a dark reddish or 
slate color. The sections are now transferred to absolute alcohol, which 
should be changed two or three times so as to dehydrate the specimen, 
which at the same time will lose much of its color. Finally the 
decolorization is completed and the section cleared up by oil of cloves, 
and it may then be mounted in balsam. Very little color should be 
visible to the naked eye in the specimen when it is ready to mount. If 
the specimen have been imbedded in celloidin for the purpose of section- 
cutting, this will be dissolved from the sections by the oil of cloves. 
Then it is well to use a second portion of oil of cloves, so as to get rid of 
the superfluous half-dissolved celloidin. It is also well to tint the oil of 
cloves lightly with a few drops of alcoholic solution of eosin, and then 
the violet-colored bacteria will stand out in sharp contrast with the 
reddish tissue elements. 

It should always be borne in mind in staining the bacteria that great 
exactness is not necessary either in preparing the coloring solutions or 
in the time of exposure of the bacteria to them. We are seeking for 
certain effects — namely, the staining of the germs — and this depends not 
only upon the quality and strength of the dye, the time of exposure, etc., 
but also upon the nature of the bacterial species and its condition at the 
time the staining is attempted. Thus it not infrequently happens that 
bacteria which will stain readily and deeply with a given solution when 
they are in a condition of active growth, may scarcely be at all colored 
if they have been dead or inactive for a long time, although their out- 
ward shape appears to be unchanged. So it should be remembered that, 
while there is little difficulty in most cases in staining the bacteria, the 
operation is not one of mere routine, but requires intelligent attention 
to the particular conditions of the species in hand. 

The Microscope. — For the recognition and study of bacteria, espe- 
cially of the minuter forms, the best optical apparatus is requisite. 



VEGETABLE PARASITES. 



Good dry lenses will answer im many cases; but for finer work homo- 
geneous immersion lenses (at least one-twelfth) must be employed. 

A special mode of illumination is also in many cases requisite, such as 
may be obtained by the use of the Abbe condenser. The structural out- 
lines which the tissue elements present, in many cases greatly interfere 
with the observation of the color by which the stained bacteria are 
recognized. This interference is considerably reduced by mounting the 
specimens in balsam; but usually not sufficiently so for the study of the 
minuter forms. The Abbe condenser is a combination of lenses, placed 
close beneath the object, by means of which, owing to the direction in 
which the rays of light are brought upon the object, structural outlines 
are made to nearly entirely disappear, and in this way the stained ob- 
jects, the bacteria, stand out much more distinctly than would otherwise 
be the case against the nearly homogeneous background. 

Artificial Cultivation of Bacteria. — For the complete investigation 
of the different forms of bacteria, particularly in their relations to dis- 
ease, we must study their life history and the effects of their inoculation 
into healthy animals. It has long been known that bacteria could be 
cultivated in a variety of artificially compounded, so-called nutrient 
media or soils. Fluids were formerly used for this purpose, but it is 
very difficult to separate single species in fluid media, and to detect 
contaminations when they occur. Moreover, the inevitable mechanical 
disturbances of the fluid prevent, for the most part, the formation 
of gross characteristic appearances in the masses of growing bacteria. 
Dr. Robert Koch introduced, a few years ago, a technical improvement 
of inestimable value, in suggesting and formulating the details of 
using solid media for the cultivation of bacteria. Among these may 
be mentioned sterilized boiled potatoes and gelatinized infusions of 
various natural or artificially compounded substances sterilized by 
heat. Different species of bacteria often require different nutrient 
media, and some require different temperatures for their most flourish- 
ing growth. They usually grow on the surface of the nutrient media in 
sharply circumscribed masses, and different species may grow side b} r 
side in the same receptacle for considerable periods, without in the 
slightest degree interfering with one another or tending to mix. The 
mode of growth and general appearances of the proliferating bacterial 
masses on the solid medium often present very characteristic differences 
between different forms, and thus not only furnish valuable means of 
identifying species, but render possible an early detection of contami- 
nation from chance admixture of species. A given species of bacteria- 
may be cultivated through a series of generations by transferring, with 
proper precautions, a minute portion from a growing colony to a fresh 
surface of sterilized soil. After cultivation through several generations, 
the species maybe presumed, and by microscopical examinations proved, 



100 VEGETABLE PARASITES. 

to be entirely pure, and the effects, if any, produced by its inoculation 
into healthy animals, to be due to it alone. 

The Preparation and Use of Culture Substances. — There are many 
culture media, some of which are best suited for one, some for another 
species of bacteria Those most commonly used are beef-tea, beef-tea 
rendered solid by gelatin or agar-agar (called "nutrient gelatin," or 
" nutrient agar "), boiled potatoes, coagulated blood serum, and milk. 

Potatoes. — The potato is scrubbed with a brush under the water 
faucet and the ends cut off with a knife, leaving a segment about an inch 
and a half long. With a tin cylinder about an inch in diameter, made 
like an apple corer, a cylinder is cut lengthwise out of the potato seg- 
ment, and this is divided lengthwise with the knife into two oblique 
sections. These pieces of potato are now placed, the narrow end up, in 
large test tubes about five inches long and a little more than an inch 
wide, which have been plugged at the mouth with cotton, and freed from 
all germs which might have been upon or in them, i.e., sterilized by heat- 
ing in an oven for an hour at 160° C. Several of the potato tubes thus 




Fig. 32.— A Potato Culture, 

Growing in a sterilized tube plugged with cotton. The red mass or "colony' 1 on the oblique 
surface of the potato is made up of myriads of bacteria. 

prepared are now put together into an open-wire basket and steamed for 
an hour, and again for an hour on the following day. They are now ready 
to be sown with the bacteria on the oblique surfaces (see Fig. 32). 

Nutrient Gelatin. — One pound of lean beef is chopped fine, stirred 
into one litre of water, covered, and set away in the refrigerator for 
twelve hours. The red fluid is now completely separated from the meat 
by squeezing through a cloth into an enamelled saucepan, which fits into 
a larger vessel serving as a water-bath. To the beef juice are added ten 
per cent of clear French gelatin, one per cent beef-peptone, and one-half 
per cent of common salt. The mixture is now heated in the water-bath 
until the gelatin is dissolved, when it is carefully neutralized by the 
addition of a sufficient quantity of an aqueous solution of sodium carbo- 
nate. It should be made exactly neutral or very slightly alkaline. The 
white of two eggs well beaten is now added, and the whole, boiled vigor- 
ously for half an hour. It is then filtered through a thick layer of 
sterilized cotton into a flask, and should form a perfectly clear, slightly 
yellowish mass which is quite firm and solid on cooling. It is now filled 



VEGETABLE PARASITES. 101 

into sterilized test tubes which have been plugged with cotton before 
sterilizing — about two inches in depth of the material being put into 
each tube — and these are steamed for from twenty minutes to half an 
hour, and again for an equal period on the following day, when they are 
ready for use (see Fig. 33). 

Nutrient Agar. — This is made and filled into tubes in the same way 
as the nutrient gelatin, save that one per cent of the agar is added in 
place of the gelatin. As the agar is less readily soluble than the gela- 
tin, it will have to be boiled longer on the water-bath before neutraliz- 
ing. After the last sterilization, the agar tubes are placed in a slanting 
position to cool, so that the agar may present a long, oblique surface. 

The Beef Tea is made in the same way, save that no solidifying 
material is added, and it may be filtered through paper. 

The Milh is prepared by filling it into test tubes (about the same 
amount as in the case of gelatin), and steaming for an hour on two 
successive davs. 




Fig 33.— A Gelatin Tube Culture. 

The bacterial growth is confined to the seat of inoculation, i.e., the surf ace and the line of needle 
puncture below. 

The mode of preparing blood serum need not be considered here. 

Having thus seen how the nutrient media are prepared, let us see 
briefly how they are used in studying the bacteria. 

In the first place, it is necessary to get from the various mixtures of 
several species, as they apt to occur in nature or in diseased parts, single 
species growing by themselves, so that their life history and characters 
may be studied in detail. To show by an example how this is done, we 
will suppose that we have a sample of water containing bacteria, and 
wish to learn how many there are and of what species, and to get them 
into separate receptacles for study. We melt the gelatin in one of the 
test tubes which we know to contain no living bacteria — because we have 
sterilized both the tube and its contents by heat — and add to it a 
measured volume, usually one c.c, of the water, and mix them by shak- 
ing; we now take a glass plate which has been sterilized by heat, lay it 
upon a cold surface, and pour out the mixture of water and nutrient 
gelatin in a thin layer upon it. When the gelatin solidifies, the invisible 
germs which the water contained are caught and held in position by it, 
and if the whole be now set away in a sufficiently warm place the living 
bacteria will presently commence to grow. 

After a few hours or days, from each one of the single living bacteria 



102 



VEGETABLE PARASITES. 



\ 



scattered through the gelatin so many new germs may have developed 
that they form a mass, called a colony, large enough to be visible to the 
naked eye. As different species grow in different ways, some forming 
colored colonies, some fluidifying the gelatin, some growing much more 
rapidly than others (see Fig. 34), we can usually recognize the different 
species either with the naked eye or under the microscope, and with a 
fine sterilized needle can pick out portions of the' different colonies and 
transfer them to the tubes of nutrient media of one kind or another 
which we have prepared, and study their growth there in the form of 
pure cultures. 

The transfer to the tubes is made by plunging the needle which has 
touched the plate colonies down into the gelatin or agar, or drawing it 




Fig. 34.— A Gelatin Plate Culture. . 
Showing bacterial colonies of various species. This plate was made by mixing 1 c.c. of the 
ordinary drinking water of New York City with the nutrient gelatin, and allowing the bacteria to 
grow for two days. 

over the surface of the potato. This is called inoculating the culture 
media. 

By the use of this principle of the plate culture, sometimes with one 
form of culture medium, sometimes with another, and with various modi- 
fications of the technique, we can separate the bacteria which occur in 
the body in disease, and, by combining animal inoculations with our 
other observations, can collect the data which enable us to decide 
whether the bacteria which are associated with certain lesions actually 
cause them. 

The most scrupulous care is required in sterilizing the nutrient 
media and the utensils and instruments used, and the greatest caution 
should be exercised, in transferring the bacteria from one receptacle to 



VEGETABLE PARASITES. 103 

another, to prevent contamination. A large experience in this sort of 
manipulation is necessary before reliable results can be obtained in 
original investigation, since the slightest error or carelessness in manipu- 
lation, or failure to observe the occurrence of contamination, is liable to 
entirely vitiate the results of long series of experiments. It is only by 
an extended preliminary training in the cultivation of some of the more 
characteristic and easily recognizable forms, under a variety of condi- 
tions, in a perfectly pure state, through a series of generations, that one 
can be assured of his capacity to carry on researches in this most difficult 
and intricate field. 

The methods of inoculation of animals with pure cultures, and the 
precautions to be observed, as well as a description of the various forms 
of apparatus made use of in practical bacteriology, must be sought in 
more extended treatises on this subject. 

It is wiser for one purposing to carry on bacterial researches to gain 
a practical acquaintance with methods and apparatus in a well-appointed 
laboratory, than to make the attempt to work out the methods from 
books. 

Material obtained from the human body which is to be subjected to 
bacterial examination should be collected with every precaution against 
accidental contamination: if fluid, in sterilized vessels; if solid, wrapped 
in cloths saturated with 1:1,000 corrosive sublimate solution, and 
brought at the earliest possible moment to the laboratory. 1 

1 Bibliography. — The most useful work for general purposes is that by Flugge on 
"Micro-organisms," 1886, in which will be found an excellent bibliography. The 
most complete treatise on bacterial technology is Hueppe's " Methoden der Bakterien- 
forschung," 1889. Most valuable also are the publications of Koch, among which 
especially to be noted are " Wundinfectionskrankheiten," Leipzig, 1878; English 
translation, "Traumatic Infective Diseases," Sydenham Soc, 1880; and ' ' Mittheilung 
a. d. k. Gesundheitsamte," Berlin, 1881, vol. i. Among the general works in English 
may be mentioned the work of Sternberg and Magnin on "Bacteria," which contains 
a bibliography and general description of various forms of bacteria, with micro-photo- 
graphs, modes of staining, etc. Crookshank's ' ' Manual of Bacteriology " contains 
tine illustrations of apparatus and cultures, and many formulae. 



INFLAMMATION. 



The condition of our knowledge is not such as to admit of an exact 
definition of the term inflammation; nor is there an entire agreement 
concerning the number of morbid changes to which this term may be 
properly applied. We have to be contented with describing the condi- 
tions which are probably of an inflammatory character. 

I. EXUDATIVE INFLAMMATION. 

We employ this term to designate a form of inflammation character- 
ized by the presence of an exudate derived from the blood-vessels. The 
vessels contain an increased quantity of blood. The plasma, the white 
cells, and the red cells escape from them and are found in the tissues. 
A portion of tissue in which such an inflammation is going on is, there- 
fore, naturally congested, swollen, hot, and tender. 

The different stages of such an exudative inflammation can be ob- 
served in animals during life. 

The transparent connective-tissue membranes of some of the lower 
animals can be studied under the microscope while inflammatory changes 
are going on. In this way we have learned that there is first a dilatation 
of the arteries, veins, and capillaries, and an increased rapidity of the 
circulation of the blood. Then the blood-current becomes slower; white 
blood-cells accumulate in the small veins and capillaries, and adhere to 
their walls. Then the white cells, changing their shape, find their way 
between the endothelial cells of the vessels, through their walls, and ap- 
pear on the outside of the vessels in the tissue (Fig. 35). This process 
is called emigration. Red blood-cells in smaller numbers may also pass 
through the walls of the capillaries and veins, and this is called diape- 
desis. At the same time the plasma of the blood transudes through the 
walls of the vessels and infiltrates the tissues as serum; while, by the 
union of substances contained in the blood plasma and in the white cells, 
fibrin is formed. 

In this simple manner are elaborated the inflammatory products — 
pus, serum, and fibrin. The pus cells are emigrated white blood-cells; 
the serum is part of the plasma of the blood; the fibrin is produced by 



INFLAMMATION. 



105 



a union of the fibrinogen in solution in the blood plasma with substances 
contained in the white blood- cells, and appears coagulated in the form, 
of granules, amorphous masses, or a reticulum. 

In order that these inflammatory products may be formed, it is evi- 
dently necessary that the blood should continue to circulate through the 
vessels of the inflamed tissue. 

Different examples of this form of inflammation give different 
amounts of inflammatory products, and also different relative propor- 
tions of serum, fibrin, and pus; while extravasated red blood-cells may 
also be intermingled with them. 

The inflammatory products may accumulate wherever there are cavi- 




Fig. 35.— Emigration of White Blood-cells in Inflamed Bladder of Frog. 



ties to receive them, in the interstices of connective tissue, on the sur- 
faces of the serous membranes, and in the serous cavities. 

The simplest form of exudative inflammation is that in which the 
changes in the blood-vessels and the production of serum, fibrin, and 
pus are associated with few or no changes in the surrounding tissues. 

Such an inflammation in connective tissue produces congestion, 
swelling, and infiltration, with serum, fibrin, and pus. 

In the mucous membranes there are congestion, swelling, emigration 
of white blood-cells, diapedesis of red blood-cells, and transudation of 
serum; the quantity of the inflammatory products is usually small. The 
production of mucus is at first arrested, afterwards increased. There 
may be increased desquamation of epithelium and the formation of 



106 



INFLAMMATION. 



superficial ulcers. When it occurs in the mucous membranes, such a 
simple exudative inflammation is usually called "acute catarrhal in- 
flammation" (Fig. 36). 

In the viscera there are more or less congestion and swelling; the 
quantity of inflammatory products is moderate; the functions of the 
viscus are apt to be deranged. 

The inflammation is of the same nature in connective tissue, the 
mucous membranes, and the viscera. The differences are due to the 
different structures of these parts. The process is always a transitory 
one, and does not change the tissues of the inflamed part. After the 
termination of the inflammation, the congestion subsides, the inflam- 
matory products are absorbed, and the parts return to their natural con- 
dition. 

A somewhat different character is given to the exudative inflamma- 
tion if there is an excessive emigration of white blood-cells. This is 
often called "purulent or suppurative inflammation." The excessive 




Fig. 36.— Pus CellsIfrom Catarrhal Inflammation of Bronchial Mucous Membrane. 



quantity of pus cells may or may not be accompanied by serum and 
fibrin. This is of more severe type than is a simple exudative inflam- 
mation. Connective tissue is simply infiltrated with the inflammatory 
products. In the mucous membranes, the pus cells are mixed with the 
mucus on the surface of the inflamed membrane. In the viscera, the 
stroma is infiltrated with the pus cells (Fig. 31). 

Exudative inflammation may be accompanied by the degeneration 
and death of tissue. The changes in the blood-vessels and the produc- 
tion of serum, fibrin, and pus are developed in their ordinary way, but 
there is added degeneration or death of portions of the tissues in which 
the inflammation is situated. 

Suppurative inflammation is due, in the majority of cases, to the 
presence and growth in the tissues of bacteria. The most common 
forms of bacteria found in connection with it are the Staphylococcus 
pyogenes aureus and albus, and the Streptococcus pyogenes. They fre- 
quently occur together in the same inflammatory process. In general, 
it may be said that while the staphylococcus tends to cause localized 
suppurative inflammations and abscesses, the streptococcus is more apt 



INFLAMMATION. 107 

to induce progressive forms of inflammation and to give rise to general 
infection of the body. 

The staphylococcus pyogenes aureus is widely distributed in the air 
and amoug dust particles, particularly in dirty inhabited regions. It is 
not readily killed by drying or freezing. It grows readily in various 
artificial culture media, assuming, when exposed to the air, a golden 
yellow color. It fluidifies gelatin. Staphylococcus pyogenes albus ap- 
pears to be simply a variety of staphylococcus, differing from the staphy- 
lococcus pyogenes aureus especially in the absence of color in the 
growths. 

The streptococcus pyogenes grows more slowly than the staphylo- 
coccus, does not fluidify gelatin, develops no color. The chain form is 
apt to be most marked in beef -tea cultures. There is much reason for 
believing that the streptococcus pyogenes is identical with the strepto- 
coccus of erysipelas and diphtheria. 

In connective tissue there are congestion, exudation of serum, emi- 
gration of white blood- cells, and death of portions of tissue. The dead 
tissue softens, breaks down, and cavities are formed which contain serum, 
pus cells, and fragments of dead tissue. Such cavities, with their con- 
tents, are called " abscesses." When healing occurs, the cavities of the 
abscesses are filled, first with granulation tissue, and afterwards with 
cicatricial tissue. 

In mucous membranes there are congestion, exudation of serum rich 
in fibrino-plastic substances, emigration of white blood-cells, and necrosis 
of tissue. The fibrin infiltrates the stroma and coagulates on the sur- 
face of the mucous membrane, so as to form false membranes. The pus 
cells are entangled in the fibrin. The necrosis involves only the epithe- 
lium, which passes into the condition of coagulation necrosis and forms 
part of the false membranes; or it involves the stroma also. The death 
of the epithelium forms superficial erosions; that of the stroma, ulcers of 
varying size and depth. Such an exudative inflammation of the mucous 
membranes is called "croupous" or "diphtheritic" (Fig. 37). 

In the mucous membranes, when healing occurs, the dead epithelial 
cells may be replaced by new cells of the same kind, but the ulcers 
formed by the death of the stroma have to be filled by granulation 
tissue. 

In the viscera, the congestion is more or less marked, and there are 
exudation of albuminous serum and emigration of white blood-cells. 
At the same time the cells of the viscus undergo degenerative changes; 
they are swollen, or coarsely granular, or broken down. There may 
also be death of portions of the stroma, with groups of cells and the 
formation of abscesses. In recovery, the degenerated cells may be re- 
placed by new visceral cells, and the abscess cavities are filled by granu- 
lation tissue. 



108 



INFLAMMATION. 



This variety of exudative inflammation is of severe type, is accompa- 
nied with marked symptoms, and, after it has subsided, leaves changes 
in the tissues. 



^^&m^mM0ml^^^m^^S 




Fig. 37.— Croupous Inflammation of Trachea. 
In this case there is purulent infiltration of the mucosa and submucosa, and of portions of the 
mucous glands, a, false membrane ; b, portion of intact epithelium ; c, infiltration of the mucosa 
with fibrin ; d, portion of mucous gland infiltrated with pus. 

Exudative inflammation may be accompanied or followed by the pro- 




Fig. 38. — Granulation Tissue from Wound of Skin. 

duction of new tissue. The congestion and the exudation of serum, 
fibrin, and pus are well marked, but from the very first there is also a 



INFLAMMATION. 



109 



formation of new tissue. This new tissue is composed simply of small 
cells with a scanty basement substance between them — indifferent tissue. 
Or it is composed of cells like the white cells of the blood, small poly- 
gonal cells with a large nucleus, fusiform and branched cells, large epi- 
thelioid cells, a basement substance and blood-vessels — granulation tis- 
sue (Fig. 38). 

The basement substance is at first scanty and homogeneous or finely 
granular. As the granulation tissue grows older, it becomes more abun- 
dant, denser, and fibrillated. 

The blood-vessels are very numerous and at first thin-walled. They 
are formed from the original blood-vessels of the connective tissue by 
the outgrowth of solid sprouts of protoplasm which afterwards become 
channelled, so that the blood passes into them, and changed so as to form 
a wall of endothelial cells (Fig. 39). 




Fig. 40. 

-Developing Blood-vessels in New-formed Tissues. 
Fig. 40.— Cicatricial Tissue. 

The surface of such granulation tissue is dry, or coated with serum, 
pus, or fibrin. 

It may remain in the condition of granulation tissue for an indefinite 
length of time, or it may be gradually changed into cicatricial connec- 
tive tissue. In the latter case, the basement substance increases and 
becomes dense, the cells disappear, the new blood-vessels are obliterated, 
and there results a dense, contracted area of connective tissue (Fig. 40). 

In connective tissue, the fibrin, serum, and pus are found in varying 
quantities. The new tissue forms thickenings and adhesions. 

In the mucous membranes, the serum, fibrin, and pus are scanty; the 
new tissue thickens the stroma of the membrane; the functions of the 
mucous glands may or 'may not be changed. 

In the viscera, the quantity of the inflammatory product varies. The 



110 



INFLAMMATION. 



new tissue is produced in the stroma; there may also be degeneration of 
the visceral cells. In the viscera, this may be called a " diffuse inflam- 
mation/' 

The most marked features of this form of exudative inflammation are 
its tendency to persist for a long time, the frequency with which it runs 
a subacute course, and the permanent character of the new tissue pro- 
duced. 

II. PEODUCT1VE INFLAMMATION. 

This term is used to designate a form of inflammation of which the 
product is new connective tissue, while congestion and exudation are 




Fig. 41.— Omentum op Dog, showing Cellular Peritonitis on Fourth Day, X 500 and reduced. 



nearly or entirely absent. Such an inflammation may be acute; it is 
more often chronic. Concerning the chronic forms opinions are not 
agreed. Many examples of this lesion are often called sclerosis, fibroid 
degeneration, or senile changes. In the present state of our knowledge, 
it seems to me better to include all these changes with the inflamma- 
tions. 

In acute productive inflammation, or cellular inflammation, the only 
inflammatory products are connective-tissue cells. The most frequent 
examples of this are found in the pia mater and the peritoneum (Fig. 
41). 

In chronic productive inflammation, the inflammatory product is 
new connective tissue, with an excess either of basement substance or of 



INFLAMMATION. 



Ill 



cells. The new tissue thus produced may subsequently undergo fatty 
degeneration or become calcified. 

In connective tissue, the inflammation produces thickenings and ad- 
hesions. 

In mucous membranes, the growth of new tissue is in the stroma. 
This is thickened, either diffusely or in the form of polypoid growths. 
The layer of epithelium may be thickened or thinned. The mucous 
glands are atrophied, or hypertrophied, or become cystic. The produc- 
tion of mucus is increased or diminished. Such a productive inflam- 



ed 

* - r 





8L -JT- 



^5 



NIP 


















SsafV* 



■-^". ^.^i^^^-^^ 



^%i^ ■# * ". ^ 



s.^-jfi*W^* 



Fig. 42.— A Tubercle Granulum from the Pleura, x 850 and reduced. 
The giant cells form part of the basement substance. 

mation of the mucous membranes is commonly called a "chronic ca- 
tarrhal inflammation." 

In the viscera there is a growth of indifferent tissue or of connective 
tissue in the stroma. The visceral cells are compressed, or degenerated, 
or atrophied. The functions of the viscus are seriously interfered with. 

The most marked features of this form of inflammation are its slow 
course and its tendency to continue. 

III. TUBERCTJLAK INFLAMMATION. 

Tubercular inflammation is an inflammation accompanying the pre- 
sence and growth of the tubercle bacillus (see Tuberculosis). The 



112 



INFLAMMATION. 



■ ^, ,.-.-: ■■■-■■■■ . 



-W; 




I ■ i-.m 



•• j; -ViV 





" ' ' ■ 7 ; . ~ 


p^ 






Fig. 43.— Diffuse Tubercle 




g&E&k _. ~' , 1 " ' l 


Mt 




.VI- 





1500 and reduced. 



'.J 







,y 



v ^' o'i » ' ; ^ 'J- _ i L -■ . _ i ' 



^ -v . 



Fig. 44. — A Miliary Tubercle from a Lymphatic Gland, x 850 and reduced. 
The giant cells are inclosed by the basement substance. 



INFLAMMATION . 113 

inflammation itself is of the exudative or productive type, or of both 
combined. 

The exudative form of inflammation is accompanied with the produc- 
tion of serum, fibrin, and pus. 

The productive form is accompanied with the production of round- 
celled tissue, of fibrous tissue, or of tubercle tissue (Fig. 42). Tubercle 
tissue is composed of a basement substance forming a meshwork inclos- 
ing large polygonal cells, and of giant cells. It is arranged in the form 
of little spherical bodies — tubercle granula — or of diffuse infiltrations 
(Fig. 43). 

With tubercular inflammations there is often associated obliterating 
endarteritis. The new tissue produced is of low vitality, so we find that 
tubercular inflammations are regularly attended with necrosis and cheesy 
degeneration. 

There is also a well-marked disposition on the part of tubercular in- 
flammation to continue and to become chronic. 

Tubercular inflammation may be diffuse, involving large areas of 
tissue; or it may be circumscribed, involving a number of small areas. 
In the latter case, the little foci composed of products of inflammation 
are called miliary tubercles (Fig. 44). 

IY. SYPHILITIC INFLAMMATION. 

Syphilitic inflammation is an inflammation caused by the poison of 
syphilis, and very probably accompanied by the growth of some specific 
micro-organism, the nature of which we do not yet know. The inflam- 
mation is of the exudative or productive type, or of both combined. 

The new tissue is either connective tissue, or small round-celled 
tissue, or granulation tissue. The connective tissue is especially com- 
mon in the viscera, taking the form of an interstitial inflammation. 
The small round-celled tissue and granulation tissue are produced in 
connective tissue, in the mucous membranes, and in the viscera, usually in 
the form of circumscribed masses called " gummy tumors," or, in the 
mucous membranes, "mucous patches/' These new tissues possess but 
few blood-vessels. The vessels in the surrounding tissue are changed 
by endarteritis. Coagulation necrosis and degeneration soon begin to 
involve the new tissue. 

ACUTE DEGENERATION. 

The introduction into the body of certain poisons, such as arsenic, 
phosphorus, and mercury, and of the poisons of the infectious diseases, 
is regularly followed by acute degeneration or death of the cells of the 
viscera. 

A small quantity of one of these poisons produces simply a swelling 
of the visceral cells. 



114 INFLAMMATION. 

A larger quantity not only causes the cells to become swollen, but 
they are also infiltrated with granules of albuminoid matter and of fat, 
and are prone to disintegrate and break down. To these changes may 
be added a secondary exudative inflammation. 

In the more intense forms of poisoning, there is a rapid death of the 
visceral cells. They either disintegrate and break down, or pass into the 
condition of coagulation necrosis, With such a rapid death of the cells, 
a well-marked secondary exudative inflammation is often present. 

Some of the examples of such acute degeneration are often called by 
the name of "parenchymatous inflammation." 









TUMORS. 



SECTION I. GENERAL CHARACTERS. 

Tumors are composed of the same types of tissue as those normally 
existing in the body, and from the latter they are derived by a prolifera- 
tion of pre-existing cells. The tissues of tumors may be similar to those 
of the part in which they grow, when they are called homologous; or 
they may be dissimilar, and are then called heterologous. Tumors are 
not only analogous to the normal tissues of the body in structure, but 
their life history transpires under the same general laws of nutrition, 
growth, reproduction, etc. With this important difference, however: 
that while the normal tissues, serving as they do a definite purpose in 
the organism, are closely limited in their growth and minute characters 
by physical and other conditions which determine the uniform develop- 
ment and correlation of various parts, the tissues of tumors exhibit a 
certain lawlessness in growth, structure, and life history which gives 
them a distinctive character while not removing them from the physio- 
logical types. Thus in the Ohondromata, 1 the tissue, while distinctly 
cartilaginous in type, presents itself not only in places where it does not 
belong, but may show a tendency to the development of fibres in one 
part of its basement substance, while another may be distinctly hyaline, 
or another soft and almost gelatinous. The cells also are apt to exhibit 
great lack of uniformity in size, shape, and grouping. The lawlessness 
in tumor tissues is shown in their tendency, under certain conditions, 
to change from one form into another, as from fibrous tissue into bone. 

Tumors are supplied with blood-vessels which grow into them from 
adjacent healthy parts, just as they do into granulation tissue, so that 
they may finally possess a more or less independent vascular system of 
arteries/capillaries, and veins. They are furnished with lymph vessels 
and some of them with nerves. The cell division by which tumors grow 
exhibits the same minute phenomena as does cell division in normal 
tissues. Tumor tissues are subject to the same degenerative changes as 
other tissues; they may become fatty or calcified, ulcerated, gangrenous, 

1 Tumors are designated by the termination oma (plural omata). 



116 TUMORS. 

pigmented, etc. By necrotic changes a tumor may be largely destroyed, 
but complete obliteration rarely occurs in this way. They are liable 
to undergo the ordinal inflammatory changes, granulation tissue may 
form in them, and abscesses and cicatrices. 

The rapidity of growth of tumors varies greatly; some grow very 
slowly indeed, and may change but imperceptibly in size and appearance 
for years, while others, on the other hand, grow so fast that they do not 
acquire solidity, and their elements remain in an incompletely developed 
condition, and are thus more liable to destructive changes than normal 
tissues are. In healthy tissues, the blood-vessels are supported by sur- 
rounding elements, which aid them in sustaining the blood-pressure 
from within. In rapidly growing tumors, this external support is often 
lacking, and, as the walls of the blood-vessels are themselves badly 
formed, the result is that the walls are apt to become pouched or aneu- 
rismal, and they often burst, giving rise to larger or smaller interstitial 
haemorrhages. 

Tumors have various shapes: nodular, tuberous, fungoid, polypoid, 
papillary, dendritic, etc. 

Tumors may occur singly or in greater or less numbers in the same 
or in different parts of the body. If they are multiple, they may have 
occurred simultaneously or at different times as independent structures. 
Or multiple tumors may occur as the result of the dissemination in the 
body, from a primary tumor, of cells which form a starting-point for 
new tumors. Many tumors are sharply circumscribed, may be even 
incapsulated, and influence surrounding parts only by the pressure 
which they exert upon them. In this way they may cause displace- 
ment, atrophy, or necrosis; they may, by pressure on neighboring ves- 
sels, cause oedema, thrombosis, etc. ; they may in the same way cause 
dislocation and caries of bones. / 

Tumors may grow largely by increase of elements within them, thus 
simply expanding; this is called central growth. They may grow in 
part or largely at the surface— peripheral growth. In this case the 
growth may be a direct, continuous enlargement of the mass at or near 
the periphery, or it may be by the formation of secondary nodules near 
the primary growth, which, gradually enlarging, finally coalesce with the 
latter, forming a part of the nodular tumor. This mode of enlargement 
is called discontinuous peripheral growth, and is due to the dissemina- 
tion of cells from the mother tumor into the adjacent tissue, through 
the blood or lymph channels, and their proliferation at the points of 
lodgment. This dissemination may occur by the agency of blood or 
lymph currents or by the amoeboid movements of the cells. 

It is not yet certain whether the new cells which are produced in 
tumors are altogether the result of the proliferation of the primary 
tumor cells, or whether the ordinary tissue cells of the part, connective- 



TUMORS. 117 

tissue cells, white blood-cells, etc., may undergo transformation and 
proliferation under the influence of the characteristic cells of the tumor. 
It is not unlikely that both modes of increase occur, although the former' 
is probably the more common and important. Some tumors increase by 
an infiltration of surrounding tissues, whose elements they gradually 
replace. In certain tumors, the old tissue of the part in which they 
grow may remain with its vessels, and form a sort of matrix whose in- 
terstices are infiltrated with the new tumor tissue. The irritation of 
the tumor may induce inflammatory new formation of tissue of the old 
matrix about or within the tumor. 

But all tumors are not limited to that part or region of the body in 
which they first occur. Sooner or later, secondary nodules resembling 
the first may be found in the most distant parts of the body, sometimes 
singly, sometimes in great numbers. These may grow like the parent 
tumor, and themselves form foci for new disseminations. 

This dissemination of tumors is one of the most important elements 
of malignancy, and is called metastasis, the secondary tumors being 
called metastatic tumors. This occurs by the transportation of tumor 
cells through the blood or lymph channels. Since the tumor itself may 
be filled with new and badly formed blood and lymph vessels, and its 
structures be in close contact with the vessels of the tissue in which it 
grows, the cells of the primary tumor may, by ulceration through, or by 
atrophy of, the walls, readily find their way into the lumen of the ves- 
sels, and be swept away by currents as emboli, and, finding lodgment, 
proliferate and grow, forming secondary tumors; or the proliferation 
may occur in the vascular endothelium itself, when the formation of 
emboli is easy to understand. When carried through the lymph ves- 
sels, the tumor cells may for some time be kept from the larger chan- 
nels and from general dissemination by lodgment in the lymph glands, 
where they may establish independent tumors. The parts of the body in 
which metastatic tumors are most apt to form depend, of course, upon 
the situation of the primary tumor and the distribution of the vascular 
channels through which dissemination occurs. 

The tumors in which metastasis is most apt to occur are, as a rule, 
those which grow rapidly, are vascular and succulent, and contain many 
cells. 

Not less variable than the size, mode of growth, and structure of tumors 
is their significance in the organism. Surgeons have in the past, and to 
a certain extent still do classify tumors, for practical purposes, as malig- 
nant and benign, and for a long time malignant tumor and cancer were 
synonymous terms. Now we know that other tumors as well as cancers 
are malignant, and, furthermore, contrary to the former belief, that ma- 
lignancy does not depend upon any specific agent in the tumor. If we 
mean by a malignant tumor one which may cause death, any tumor may 



118 TUMORS. 

be malignant if growing in the right place. Thus a simple fat tumor, 
by pressing on the trachea, may cause suffocation, and any tumor may 
secondarily cause death by haemorrhage or septicaemia. The real signs 
of malignancy in a tumor are: 1. Invasion of adjacent tissues by eccen- 
tric or peripheral growth. 2. The tendency to local recurrence after 
removal. 3. The formation of metastases. 4. A tendency to interfere 
with the nutrition and general well-being of the body, which may give 
rise to a condition known as cachexia. The modes of invasion of sur- 
rounding tissues and the formation of metastases have been considered 
above/ The tendency to local recurrence after removal is probably, in 
most if not all cases, due to the incomplete removal of the peripheral 
infiltrating cells. These may be very few in number and lacking in 
characteristic structural features, but are none the less endowed with the 
capacity of proliferation and development into a new and similar tumor 
at or near the seat of the extirpated One. The infiltrating peripheral 
cells may remain dormant for a long time after an operation, or may im- 
mediately commence to grow. The mere fact that a second tumor de- 
velops in the place of one removed does not imply malignancy, since it 
may result from the same mechanical cause which produced the first, as 
in the case of certain carcinomata of the lip induced by the mechanical 
irritation of a pipe. 

The drain upon the system by the rapid growth of a tumor, together 
with the absorption from it into the body of deleterious putrefactive 
materials, from sloughing, ulceration, and degeneration, may give rise 
to fever and other constitutional disturbances. Or they may induce 
feebleness, anaemia, and that general impairment of the nutritive func- 
tions of the body known as cachexia. This condition is frequently ren- 
dered worse by the mental status of the patient in the presence of such a 
traditional object of alarm. 

It should be remembered, however, that so long as they are localized 
and have not undergone degenerative changes, even the most malignant 
tumors do not usually give rise to a cachexia, since the drain upon the 
nutritive powers of the system by their simple growth is not, under ordi- 
nary conditions, very considerable. When the system is deteriorated by 
the absorption of septic materials from tissue degeneration, however, 
this may become a very important factor. 

This condition of cachexia, so evidently secondary to the growth and 
degeneration of the tumor, was formerly termed a dyscrasia or diathesis, 
and was supposed to precede and induce the growth of malignant tu- 
mors, particularly cancers. 

It is further to be noted that the fragments of tumors which have 
found access to the veins may act as simple emboli and produce imme- 
diate death, or simple metastatic abscesses. 



TUMORS. 119 



THE CAUSE OF TUMORS. 



In regard to the causation of tumors, our actual knowledge is still 
very meagre. In a certain number of cases, mechanical influences are 
undoubtedly sufficient inciting causes. In other instances, heredity is an 
important factor. But to both of these influences too much importance 
has been attributed informer times. The most recent, and to a certain 
extent plausible, hypothesis, and one which most satisfactorily accounts 
for the occurrence and character of many tumors, is that of Cohnheim, 
called the hypothesis of the embryonal origin of tumors. This is to the 
effect that all true tumors are due to faulty embryonal development; 
that certain embryonal cells of various kinds, in the course of the devel- 
opment of the body, are superfluous, or become displaced, or do not un- 
dergo the normal changes, and remain ready, when the conditions shall 
become favorable in later life, from whatever reason, to commence 
growing with all the potencies of embryonic and lowly organized cells in 
the midst of the mature tissues. ISTot being restrained, however, by the 
regulating influences which determine the nature and relative extent of 
growth in normal development, they go on to the production of tumors, 
which represent, though in atypical form, the various tissues which 
the strayed or unused cells were destined normally to produce. 

The evident hereditary character of many tumors, the congenital 
nature and early development of others, their atypical structure in 
general, and the tendency of many forms to occur in situations in which, 
during the development of the embryo, considerable complexity exists, 
as well as their heterologous occurrence and their frequent primary 
multiplicity — all of these characters of tumors seem to favor Cohn- 
heim's hypothesis. On the other hand, the theory leaves unex- 
plained the sudden growth of the alleged germs which have long re- 
mained dormant, and lacks as yet the absolute demonstration of a 
morphological basis, since no one has seen the strayed or delayed em- 
bryonic cells. These may, of course, be very small and difficult of 
demonstration, and this, according to Cohnheim, fully explains the lack 
of a definite histological basis to his hypothesis. It should be remem- 
bered, furthermore, that, under ordinary conditions in the body, certain 
cells which are destined to replace others which have fulfilled their 
destinies, as in the skin, possess to a greater or less degree the characters 
of embryonal cells, and that, while in the struggle for existence the 
growth of these cells may be held in check, as by conditions of pressure, 
nutritive supply, etc., if these conditions be altered these cells may 
undergo proliferative changes as significant as those of the alleged 
belated germs of Cohnheim. Such a changed condition of affairs has 
been shown by Thiersch to occur frequently in the skin in old age, and 
to explain in large measure the occurrence of certain epithelial tumors. 



120 TUMORS. 

It should be remembered that this hypothesis was offered by Cohnheim 
only as a suggestion to facilitate research, and that he expressly warned 
his confreres against attaching a premature importance to the possibility 
to which he called attention. Thus, while the hypothesis of the em- 
bryonal origin of tumors is most fascinating, and for certain forms quite 
satisfactory, we may well demand a more definite basis of fact before 
accepting it as of universal application. 

It was formerly supposed, when the doctrine of the specific nature 
of tumors prevailed, that the cells of malignant tumors, particularly of 
cancer, had a characteristic structure and appearance, and that by the 
examination of single or of a few separated cells the nature of the tumor 
could be determined. From the above considerations, it will be evident, 
as all tumor cells have their prototypes in the normal body, that there- 
fore there is nothing pathognomonic in the appearances of single cells. 
It is by a study of the general structure and of the topography of tumors, 
as well as of the characters of the individual cells, that we are enabled 
to determine their nature. And even then we must often bring to our 
aid the clinical history and gross appearances of the growth before we can 
arrive at a definite conclusion. We may, indeed, sometimes, aided by the 
clinical history or gross appearances, be able, by the microscopical exami- 
nation of scrapings from a tumor or of fluids from an internal cavity in 
which it is growing, to form a reasonable conjecture regarding its nature. 

As a rule, the peripheral portions of the more rapidly growing tumors 
are best adapted for microscopical examination, because here secondary 
degenerative changes are less likely to have occurred than in the central 
parts. 

Bacteria have in recent times been claimed by some observers to 
stand in a causative relation to certain tumors, and bacteria have been 
occasionally demonstrated in, and cultivated from, the tissues of tumors. 
But no complete and reliable experiments or observations have as yet 
been made which prove that they have anything to do in causing the 
tumors, or are of any significance save as chance contaminations of the 
tissues or as inducing secondary complications. 

CLASSIFICATION" OF TUMORS. 

The fact that tumors are composed of structures which resemble the 
various types of tissue found in the normal body suggests the guiding 
principle in their classification. But in order to thoroughly understand 
either the classification of normal tissues or the grouping of the tumors, 
we must keep in mind the way in which the tissues are developed in the 
embryo. 

According to the more recent views of embryologists, particularly of 
His and Waldeyer, the primitive tissues of the body belong to two 
groups: those of archiblastic and those of paraMastic origin. In the 



TUMORS. 121 

early stages of foetal development, the new cells which are formed at 
first arrange themselves in three layers, to which collectively the name 
arch i blast is applied. 

Of these three archiblastic layers, the outer, called the epiblast, fur- 
nishes the material for the epithelium of the skin and its adnexa, for 
the epithelium of the terminal portions of the alimentary canal, and for 
the nervous system, including the neuroglia. 

The middle layer — the mesoblast — furnishes the material for the 
epithelium of the genito-urinary organs, and for both the smooth and 
striated muscle tissue. 

The inner layer — the hypoblast — affords the material for the devel- 
opment of the epithelium of the respiratory and the digestive systems, 
with that of the various glands and passages which develop out of and 
in connection with them. 

The exact origin of the parablast, which develops later than the 
archiblast, is still uncertain; but it furnishes the material out of which 
are formed the connective tissues, including cartilage, bone, teeth, and 
fat; the blood-cells and blood-vessels; the lymphatic tissues and lymph 
vessels, and the true endothelial cells. 

Now, if we wish to arrange in groups the different kinds of tumors 
found in the body, we have only to recall the varieties of tissue which 
normally exist there, and their grouping, and upon the classification of 
the physiological types to construct the classification of tumors. It 
should be remembered that the usual separation of the normal tissues 
into groups is useful, rather because it facilitates their study than 
because it expresses absolute and fundamental distinctions; and the 
same may be said of all the classifications of tumors. In both, an 
increase of our knowledge concerning their structure and genesis will 
doubtless lead to a more accurate grouping; but, for the present, such 
an arrangement as that indicated below will be found of practical value 
for the purposes of studying tumors. 

I. Tumors Composed of Tissues of the Type of those forming the Con- 
nective-Tissue Groicp. — Histioid or Connective-Tissue Tumors. 
Physiological Type. Tumors. 

1. Fibrillar connective tissue. 1. Fibroma. 

2. Mucous tissue. 2. Myxoma. 

3. Embryonal connective tissue. 3. Sarcoma. 

4. Endothelial cells. 4. Endothelioma. 

5. Fat tissue. 5. Lipoma. 

6. Cartilage. 6. Chondroma. 

7. Bone. 7. Osteoma. 

8. Neuroglia. 1 8. Glioma. 

1 It will be seen, from the account given above of the origin of the various tissues in 
the different embryonic layers, that the neuroglia has a different origin from the other 
JO 



122 TUMORS. 

II. Tumors Composed of Tissues of the Type of Muscle Tissue. — 

Myomata. 

Physiological Type. Tumors. 

1. Smooth muscle tissue. 1. Leiomyoma. 

2. Striated muscle tissue. 2. Rhabdomyoma. 

777. Tumors Composed of Nerve Tissue. — Neuromata. 
Physiological Type. Tumors. 

1. Nerve tissue. 1. Neuroma. 

IV. Tumors Composed of Vascular Tissue. — Angiomata. 
Physiological Type. Tumors. 

1. Blood-vessels. 1. Angioma. 

2. Lymph-vessels. 2. Lymphangioma. 

V. Tumors in which the Predominant or Characteristic Elements are 

Epithelial Cells. 

Physiological Type. Tumors. 

1. Glands. 1. Adenoma. 

2. Various forms of epithelial cells 2. Carcinoma. 

and associated tissues. 

VI. Tumors Formed by Various Combinations of the above Types. — 

Mixed Tumors. 

Aside from the above well-marked classes, we may mention here for 
the sake of completeness: 

(a) Complex Congenital Tumors — Teratoma, — These are congenital 
tumors which frequently contain a great number of different forms of 
tissue, such as various forms of fibrillar connective tissue, cartilage, bone, 
teeth, hair, skin, muscle, and glands. They are most frequently found 
at the lower end of the spine, about the head and neck, or in the gen- 
erative organs. Some of them probably arise by an inclusion of portions 
of another foetus. These are called teratoid tumors, or teratomata. 
Among them are sometimes classed other and simpler congenital forma- 
tions, such as dermoid cysts, congenital angiomata, and the so-called 
pigmented moles. 

(b) Cysts. — These structures, for the sake of convenience, are usually 
classed among the true tumors, although in general characters, struc- 
ture, and genesis they are entirely different products. They are usually 
divided into two classes: 

I. Cysts which develop in pre-existing cavities. 

II. Cysts which originate independently as the result of pathological 
changes. 

connective tissues. The neuroglia, as well as the tumors derived from it, presents 
marked peculiarities in structure, but its structural and functional alliance with the 
other connective tissues justifies its grouping among them. 



TUMOKS. 12& 

I. Cysts which develop in pre-existing cavities: 

1. Retention Cysts. — These are chiefly formed by the accumulation 
in glands or their excretory ducts of the more or less altered secretion of 
the gland. They usually occur as the result of some hindrance to the 
normal discharge, as from inflammatory contractions, pressure, etc. The 
contents of such cysts are usually mucous, sebaceous, serous, or of a 
mixed character. Their walls are the more or less altered walls of the 
original structure. To this class belong comedones, milium, atheroma, 
chalazion, ranula, the ovula Nabothi, milk cysts, and certain serous cysts 
of the ovaries. Fallopian tubes, gall-ducts, and uriniferous tubules. 

2. Exudation Cysts. — These arise usually, though not always, as the 
result of a chronic inflammatory process in lymph spaces or serous sacs, 
and among them are to be classed the so-called ganglia, hydrocele, etc. 
Certain of the so-called hematoceles, in which blood is extravasated into 
closed cavities, form a variety of the cysts of this group. 

II. Cysts which originate independently as the result of pathological 
changes: 

1. Cysts formed by the softening and disintegration of tissue. — Such 
cysts may at first be small and have very meagre contents and no well- 
defined wall. A wall may finally be present either as an entirely new- 
formed structure, or the more or less modified capsule of the organ in 
which they occur may partly or entirely form the wall. The contents of 
.such cysts are usually the more or less altered detritus of the tissue by 
whose disintegration they are formed. Such cysts are very apt to occur 
within true tumors, particularly those which are succulent and of rapid 
growth, since these, as above stated, are very liable to degeneration. Old 
abscesses may change into well-defined cysts of this kind. 

2. Cysts formed around foreign bodies. — The inflammatory reaction 
induced by the presence of foreign bodies of various kinds, parasites, 
masses of extravasated blood, etc., frequently result in the formation of 
well-defined incapsulated cysts. 

3. Cysts formed by a new groivth of tissue in whose spaces various 
kinds of fluid accumulate. — These spaces may or may not be lined with 
epithelium and have something of the glandular character. Such forms 
are exemplified in some of the compound ovarian cysts— the so-called 
ovarian cystomata. 

4. Congenital Cysts. — These are of various forms, and their mode of 
origin is in most cases but imperfectly understood. The so-called der- 
moid cysts of the subcutaneous tissue and ovary are marked examples of 
this class. Certain congenital cysts of the kidney and other internal 
organs are conveniently grouped in this class, although it is quite prob- 
able that some of them at least originate during foetal life in one or other 
of the above-described ways, and hence are not essentially different in 
nature from some of the cysts of other classes. 



124 TUMORS. 

Various Lesions sometimes described as Tumors. — There are certain 
enlargements of the lymph glands or nodes which are in reality hyper- 
plasias, sometimes inflammatory in character, and sometimes not, and 
which are often grouped among the tumors as lymphomata. They are 
not, strictly speaking, true tumors, and will be considered under the 
lesions of the lymph nodes. 

In the same group are often classed the enlargements of the lymph 
glands in leukaemia and in other general diseases, which will be treated 
in another part of this book. Another group of tumors, sometimes 
called lymphomata, are in reality sarcomata, and these will be described 
under the latter heading. 

There is also a group of nodular new formations, the so-called Infec- 
tive Granulomata, which are sometimes classed among the tumors. 
These are found in tuberculosis, leprosy, syphilis, lupus, glanders, and 
actinomycosis. They seem, however, to be more closely allied to inflam- 
matory new formations than to true tumors, and, as our knowledge re- 
garding them increases, seem more and more to be dependent upon the 
irritation caused by the presence of vegetable parasites (see section 
devoted to General Diseases). 

Nomenclature of Complex Tumors — The simple occurrence of more 
than one kind of tissue in a tumor does not make it a complex or mixed 
tumor. It is only when a special kind of tissue occurs in sufficient quan- 
tity to be of definite significance, or is of such a nature as to render its 
presence, in any amount, of importance, that we recognize its presence 
in the name. The name of mixed tumors is usually formed by joining 
the names of the tissues to be recognized. Thus a combination of fibro- 
ma and sarcoma is called fibro-sarcoma; the general rule of construction 
being that the name of the more important tissue shall serve as the sub- 
stantive which that of the less important one qualifies. It should be 
remembered, however, that the more important tissue is not always the 
one which is present in greatest amount. Thus, owing to the great 
clinical significance of carcinomatous tissue, a very large fibroma with 
a small quantity of cancer tissue intermingled would be a fibro carci- 
noma and not a carcino-fibroma. 

Preservation. — In general, tumors, like all tissues for microscopical study, should 
be cut into small pieces before immersing them in the preservative fluids, and the 
sooner they can be placed in these after removal, the better will be the preservation. 
In some cases, much may be learned from large sections of tumors together with their 
surrounding tissues. In this case, the proper part of the tumor must be preserved 
whole, and is best hardened in strong alcohol. For the ordinary routine hardening of 
tumors, Muller's fluid is probably the best agent; the hardening being completed in 
the usual way with alcohol. In many cases an interstitial injection of one-per-cent 
aqueous solution of osmic acid, or a mixture of this with equal parts of alcohol and 
water, and subsequent immersion in alcohol, secures a very perfect preservation of 
the cells. 



TUMORS. 125 

When it is desired to study the living cells of tumors — and much may be learned 
in this way — fragments should be teased in one-half -per- cent salt solution and examined 
on a warm stage. For purposes of immediate diagnosis, sections may be made of the 
frozen tissue and stained with safranin. 

SECTION II. SPECIAL FORMS OF TUMORS. 
FIBROMA. 

The fibromata are composed of fibrillar connective tissue, which, as 
in the physiological type, is sometimes dense and firm, Fibroma durum, 
and sometimes loose in texture and soft, Fibroma molle. They are usu- 
ally sharply circumscribed and are frequently incapsulated, but they 
may be diffuse and merge imperceptibly into the surrounding tissue. 
Some fibromata consist almost entirely of intercellular substance, con- 
taining but few flattened or spindle-shaped cells (Fig. 45); others contain 
very many variously shaped cells. The denser varieties usually contain but 
few blood-vessels, although they are occasionally quite vascular. Many 
of the softer varieties are very vascular. Nerves also are occasionally 
seen. The course and arrangement of the fibres in these tumors are usually 
quite irregular, often crossing and interlacing in a most complex man- 



: m 






Fig. 45.— Dense Fibroma of the Abdominal Wall. 
Some of the bands of connective-tissue fibres are cut across, others are cut lengthwise. 

ner. The fibromata are usually of slow growth, but exceptionally they 
grow very rapidly. They are benign tumors, but by pressure on impor- 
tant organs, by ulceration, or by changing into other varieties of tissue, 
they may become of serious import. Pure fibromata do not form metas- 
tases, but they are often multiple, and when so are frequently congeni- 
tal. They may, like most tumors, exhibit local recurrence when not 
fully removed. They are frequently very small and insignificant, but,, 
on the other hand, may grow to an enormous size. 

They are quite frequently combined with other kinds of tissue to 
form complex tumors. The looser, softer varieties not infrequently be- 
come (edematous, when they may closely resemble myxomata. They are 
liable to calcification, and to fatty and mucous degeneration. By me- 
taplasia they may partially change to form fibro-chondroma, fibro-lipo- 



126 



TUMORS. 



ma, fibrosarcoma, or fibro-osteoma. The latter transformation fre- 
quently occurs when they form in the periosteum. Developing as they 
do in the connective tissue, they occur in the most various parts of the 
body: in the skin and subcutaneous tissue; in intermuscular tissue and 
fasciae; in periosteum; in the nerve sheaths and intrafascicular con- 
nective tissue; in the dura mater, the interstitial tissue of organs, and in 
the mucous membranes. Many of the so-called polypi of the mucous 
membranes, some psammomata, certain forms of warts and common 
papillomata, are forms of fibroma. 

Occasionally, in the ducts of glands, fibrous polypi grow to an enor- 
mous extent, their epithelial covering keeping pace in growth with 
their development, until they form very large, irregular, loose-textured 
tumors, which often finally ulcerate. Such forms are seen in the mam- 
mary gland, where they are frequently mistaken for carcinomata, They 




Fig. 46.— Myxoma of Subcutaneous Tissue op Back. 

are called Intracanalicidar Fibromata (see Tumors of the Mamma). 
It is often difficult to distinguish between genuine fibromata and inflam- 
matory or other connective-tissue hyperplasias, such as elephantiasis, 
and perhaps the fuller knowledge of the future will show that the dis- 
tinctions are not as definite as we are now disposed to believe. 



MYXOMA, 



Mucous tissue is essentially an embryonic tissue, for in the normal 
adult it is present only in a very imperfect and atypical form in the vit- 
reous of the eye, and perhaps exceptionally in small amount about the 
heart, kidneys, and medulla of bone. 

The myxomata are thus essentially embryonic-tissue tumors. These 



TUMORS. 127 

tumors consist, in their most typical forms, of a homogeneous or finely 
fibrillated, soft, gelatinous basement substance, in which are imbedded 
a variable number of spheroidal, fusiform, branching, and often anasto- 
mosing cells (Fig. 46). They may contain few or many blood-vessels 
and nerves. By the addition of acetic acid, mucin may be precipitated 
from the basement substance. The very soft forms which contain com- 
paratively few cells and much translucent basemeut substance are called 
Myxoma gelatinoxum or M. molle. The presence of many cells renders 
them more consistent and gives them a whiter and more opaque appear- 
ance ; such forms are called M. medullar e. 

Pure myxomata are not very common. The myxomata are very apt 
to be combined with fibrillar connective tissue as fibvo-myxoma; or with 
fat tissue — Upo-myxoma; and they very frequently become sarcomatous, 
or take part in the formation of very complex tumors. They may be 
diffuse or incapsulated with fibrillar connective tissue; they are fre- 
quently very large, and may be multiple. Owing to the character of 



JmmH„ 

Fig. 47.— Myxoma growing into Abdominal Cavity. 
Showing the accumulation of fat droplets in some of the cell bodies. 

the basement substance, the blood-vessels not infrequently rupture, giv- 
ing rise to larger or smaller haemorrhages within the tumor, or to the 
formation of cysts. The cells are liable to undergo fatty degeneration 
(Fig. 47). 

Composed as they are of a type of tissue from which fat tissue is de- 
veloped in the embryo, the relations of these tumors to fat tissue are 
very intimate. They are most frequently developed in, and probably 
directly from, fat tissue, and are very often combined with it as lipo-myx- 
oma. They are also found in the subcutaneous, submucous, 'and sub- 
serous tissue, in the marrow and periosteum; in the brain and cord; in 
the sheaths and intrafascicular tissue of peripheral nerves; in intermus- 
cular septa, and in the interstitial tissue of glands, such as the mamma 
and parotid. The myxomata are in general benign; yet they are very 
prone, especially the lipomatous forms, to local recurrence. They some- 
times grow very rapidly, and sometimes, though very rarely, form me- 



128 TUMORS. 

tastases. In the not infrequent combination with sarcoma, they may- 
exhibit the most marked malignancy. Many of the polypi of mucous 
membranes are myxornata, and to this class of growths belong the so- 
called hydatid moles which sometimes develop in the villi of the chorion. 
(Edematous, loose, and cellular forms of fibrillar connective tissue so 
closely resemble some of the forms of mucous tissue that certain observ- 
ers consider them as identical. So prone are many tumors to undergo 
mucous degeneration, and so frequent are the combinations of the myx- 
omata with other forms of tumors, that it is often difficult, sometimes 
impossible, to say whether the mucous tissue in a given composite tumor 
is primary or secondary. 

SARCOMA. 

These tumors are formed on the type of connective tissue, but they 
are, as a rule, largely composed of cells; the basement substance, though 
a constant and important factor, being much less conspicuous than in 
adult connective tissue. They more closely resemble, in general, the de- 
veloping connective tissue of the embryo or the granulation tissue of 
inflammation. They are, therefore, conveniently described as present- 
ing the type of embryonal tissue. The prominent and characteristic 
cells of the sarcomata are most varied in size and shape. They may be 
fusiform or spindle-shaped, spheroidal, branched; they may be multi- 
nuclear and very large, or they may be very small and spheroidal, resem- 
bling leucocytes. The fibrillar basement substance may be present in 
such small quantity as to entirely escape a superficial observation, covered 
as it may be by the abundant cells; or it may be so abundant as to give 
the tumor the general appearance of a fibroma. It may be intimately 
intermingled with the cells in fascicles, or it may be in large open-meshed 
networks, giving to the tumor an alveolar appearance. The cells, how- 
ever, always stand in an intimate relationship to the basement substance, 
•which they sometimes reveal by fibrillar processes continuous with it. 
Blood-vessels also form a constant and important structural element in 
these tumors, being in some of them so predominating a factor that they 
give structural outline and general character to the growth. They, too, 
as in the normal connective tissue, are intimately associated with the 
basement substance and with the tumor cells. 

A single form of cells is often so predominant as to furnish a suitable 
name for the tumor, but in many cases the cell form varies greatly in 
the same growth. It may be said in general that there is a tendency to 
reproduce in these tumors some of the special characteristics of the tis- 
sues in which they originate. Thus, sarcomata of the bones are apt to 
be osteo-sarcomata; those of pigmented tissue, like the choroid, are apt 
to be pigmented sarcomata. It will be more convenient for our present 



TUMORS. 



129 



purpose to briefly describe the more common forms one after another 
than to attempt any systematic classification of them. 

It should be remembered, however, that the various forms are not 
sharply specific in character, but are apt to merge into one another and 
to intermingle in various ways. 

Sarcomata are most frequently found in the skin, subcutaneous tis- 
sue, fascias, subserous connective tissue, the marrow or periosteum, and 
in the choroid. They may also occur, though more rarely, in the dura 
mater; brain and cord; lymph nodes; in the adventitia of blood-vessels, 
and in nerve sheaths; in submucous tissue; in the uterus, and in the 
kidney. In the liver and lungs and heart they may occur by metastasis. 

They are more apt to occur at an early period in life than later. The 
cellular character, the rapid growth, the vascularity and succulence of 
many forms, the marked tendency to local recurrence, and the formation 
of metastases, stamp the sarcomata as malignant tumors. But in this 
they vary greatly; while some of the forms belong in every sense to the 




Fig. 48.— Large Spindle-celled Sarcoma of HumeruS. 

most malignant of tumors, others grow slowly, are very dense, and may 
remain localized and harmless for years. Their tendencies in this re- 
spect will be mentioned under the special forms. 

Intimately related as they are to the blood-vessels, metastasis is more 
apt to.occur through the blood than through the lymph channels, and 
consequently adjacent lymph glands are much less apt to be involved 
than in some other forms of tumor, notably the carcinomata. 

Spindle-celled Sarcoma. — The cells in these tumors maybe large — 
large spindle-celled S. (Fig. 48); or they maybe small — small spindle- 
celled S. (Fig. 49). They may consist largely of cells, or may contain 
so much intercellular fibrous tissue as to be appropriately called fibro- 
sarcoma. The cells are frequently arranged in fascicles, which sur- 
round the blood-vessels, and these fascicles may cross and interlace. 
These tumors are, as a rule, denser and firmer and less malignant than 
other forms of sarcoma, but to this there are many exceptions. They 
may be incapsulated or infiltrating. To this class belong the growths 



130 



TUMORS. 



formerly described as fibre-plastic tumors and recurrent fibroids. They 
frequently occur in the periosteum, subcutaneous tissue and muscle; in 
the uterus, and in various glands, notably in the mamma, testicle, 
thyroid, etc. These forms are among the most frequent of the sar- 
comata. 



s^^s 









^ 



-: 






Fig. 49.— Small Spindle-celled Sarcoma of Forearm. 

Round-celled Sarcoma. — Of these there are two classes — 1, small 
round-celled sarcomata, and, 2, large round-celled sarcomata. 

1. The small round-celled sarcomata consist of cells of about the size 
and appearance of lymph cells, and may have much or little intercellular 
substance, which maybe irregularly disposed or arranged in large meshes 
resembling alveoli. In many cases, so small is the quantity of inter- 




Fig. 50.— Small Round-celled Sarcoma of Liver. 



cellular substance that it is difficult of detection without special modes 
of preparation. These tumors are apt to contain many blood-vessels, and 
be very soft and succulent (Fig 50). Their growth is sometimes rapid 
and they are often very malignant. 

They most frequently occur in the connective tissue of the muscles 
and fasciae, in bone, and in lymph nodes (lymphosarcoma). They also 



TUMORS. 



131 



occur in the internal organs, not infrequently in the brain, associated 
with glioma as glio-sarcoma. 

2. In the large round-celled sarcomata (Fig. 51), the cells vary in 
size, but are usually very much larger than in the last variety. Their 
nuclei are usually large and contain prominent nucleoli. They, too, 




Fig. 51.— Large Round-celled Sarcoma of Leg. 

are often very vascular, and contain a variable quantity of basement 
substance. They are occasionally alveolar in character. They are as 
a rule less soft and malignant than the small-celled varieties. 

The round-celled sarcomata were formerly supposed, on account of 
their macroscopical and clinical resemblance to some of the soft forms of 
carcinoma, to belong to these tumors, and were called medullary cancers. 




Fig. 52.— Melano-Sarcoma prom Submaxillary Region. 



Melano- Sarcoma. — These tumors consist most frequently of spindle 
cells of various sizes, although cells of other shapes frequently occur in 
them. They are characterized by the presence in the cells, and less 
frequently in the intercellular substance, of larger and smaller particles 
of brown or black pigment (Fig. 52). The pigment is usually quite 
irregularly distributed in patches or streaks, and is located chiefly in the 



132 



TUMORS. 



cell body. They arise most frequently in the skin and in the choroid. 
Pigmented moles of the skin often form their starting points. They 
belong to the most malignant of tumors. They very readily form me- 
tastatic tumors in various parts of the body, which are, like the parent 
tumor, pigmented. 

Various forms of tumors may contain brownish pigment deposited in 
them* by the degeneration of the haemoglobin from extravasated blood; 
these should not be mistaken for melanotic sarcomata. 

Myeloid or Giant celled Sarcoma. — Tumors of this class are usually 
formed chiefly of spheroidal or fusiform cells of variable size, but their 
characteristic feature is the presence of larger and smaller multinuclear 




Fig. 53.— Giant-celled Sarcoma of Bone. 



•cells, called giant cells. These are closely intermingled with the other 
cells, and may be very abundant or very few in number (Fig. 53). Giant 
cells may occasionally occur in other tumors, but are most abundant 
and characteristic in these. They are chiefly formed in connection with 
bone, and may commence in the marrow or in the periosteum. They 
are sometimes very soft and vascular, and subject to interstitial haemor- 
rhages. Some of these vascular sarcomata were formerly classed to- 
gether with other kinds of vascular tumors as fungus haematodes. 
Some of the forms of epulis are giant-celled sarcomata. 

When these tumors originate in the marrow of the long bones, which 
is a favorite place for them, they are apt to cause resorption of the bone, 
and although the tumor may be for a long time inclosed by a shell of 
new-formed bone, which enlarges with the enlarging tumor, it usually, 



TUMORS. 



133 



sooner or later, breaks through this and infiltrates adjacent tissues. 
They are liable to form metastases and frequently grow to a very great 
size. The periosteal forms are apt to be firmer in texture, and are 
prone to the development of irregular masses of new bone within them, 
thus forming one of the varieties of osteo-sarcoma. 

Osteo- Sarcoma. — These are spindle or round-celled tumors, usu- 
ally, but not always, connected with bone, in which irregular masses of 
bone tissue are present. The bone is usually of irregular atypical struc- 
ture; the regular lamellation and typical Haversian canals being usually 
absent. They may form metastases which present similar characters. 

Calcification, which should be distinguished from ossification, may 
occur in various forms of sarcoma. 

Angio- Sarcoma. — In many of the sarcomata in various parts of the 
body, the blood-vessels form so prominent and important a feature as to 




Fig. 54— Angio-Sarcoma of Liver. 
The thin-walled blood-vessels, around which the tumor cells are grouped, are irregularly 
dilated. 

give special character to the growth, not alone by their size and general 
prominence, but sometimes by the peculiar arrangement which their 
presence gives to the cells. While in most of the sarcomata the blood- 
vessels have a very important influence in determining the topography 
of the tumor, in most of the denser, and in many of the softer varieties, 
this influence is not easily traced. In many forms, however, particu- 
larly those which are soft and very cellular, the cells are closely grouped 
around the vessels, as if they were developed in their adventitise and had 
formed close sheaths around them. The masses of cells thus formed, 
with a blood-vessel for a centre, may be closely packed together in long 
strings with more or less frequent anastomoses (Fig. 54), or they may be 



134 



TUMORS. 



arranged in rounded groups, giving to the tumor an alveolar appear- 
ance. 

In other cases, the blood-vessels may appear as characteristic factors 
simply on account of their size or relative abundance. 

Sometimes the walls of the blood-vessels and the adjacent tissues, in 
these as in other forms of tumors, undergo a peculiar hyaline degenera- 
tion, giving to the whole or to parts of the tumor a more or less gelati- 
nous appearance. Such tumors are not very common, and are frequently 
grouped in an ill-defined class called cylindroma. 

Alveolar Sarcoma. — Sometimes, as above stated, the basement sub- 
stance of the sarcomata, particularly in some of the round-celled varie- 
ties, is quite abundant and arranged in a wide-meshed net, in the 
meshes of which the cells lie. These spaces are called alveoli, and this 
variety of structure has acquired importance from the general resem- 




Fig. 55. Myxo-Sarcoma of Pharynx. 



blance which these tumors have to the well-defined and characteristic 
alveolar structure which many of the carcinomata exhibit. It is true 
that occasionally the resemblance is very close indeed, but usually the 
sarcomata present a more or less intimate relation between the cells and 
basement substance. The cells usually do not simply lie in the cavities, 
but are often attached to the intercellular substance, which not seldom 
sends finer trabecule into the alveoli between the cells. Sometimes a 
careful shaking of sections in water is necessary to reveal the characters 
of the reticulum. The cells, moreover, are usually, though not always, 
distinctive in character. This form of tumor is, in some cases at least, 
determined, as above stated, by the new formation and peculiar arrange- 
ment of the blood-vessels. Tumors of this kind are not common, but, 



TUMORS. 



135 



may occur in the skin, lymph nodes, bones, and pia mater. They are 
usually very malignant. 

In addition to the above more or less well-defined forms of sarcoma, 
there exist various modifications which have received special names. 
Thus sarcomata in which cysts form, either by the softening of tissue by 
degeneration, or by the dilatation of gland ducts by pressure, or by the 
new formation of tissue in gland ducts or alveoli which dilate with the 
growth of the tumor, have received the name of cysto sarcomata. 

Mucous degeneration is frequent in the various forms of sarcoma. 
A combination of myxoma and sarcoma — myxo sarcoma — is common 
(see Fig. 55). 

Combinations of sarcoma with fat tissue, Uposarcoma; with glandular 
structures, adenosarcoma (Fig. 56); with cartilage, chondrosarcoma; 







4; '»/ ' i' '■' < ■ 

m ■- &,' •£.-''.'■'/ ; it. ■-'■- - .C-. ' , 






fc"V, 



Fig. 56.— Adeno-Sarcoma of Parotid. 

with muscle tissue, myosarcoma ; and with various other tissues, are of 
frequent occurrence. Some forms of psammoma, or " brain sand," found 
chiefly in the dura mater, are jibro sarcomata which have undergone 
calcification, the lime being deposited in lamellated masses of various 
shapes within them. 

Some of the soft papillomata and warts, and occasionally the polypi 
of the mucous membranes, belong to the type of sarcoma or myxo- 
sarcoma. 

The so-called chloromata, which have been found in a variety of 
places in the body, but are rare, are apparently forms of sarcoma. Chlo- 
roma is characterized by a greenish color the nature of which is not 
known. 

Sometimes in various forms of sarcoma, as in other tumors, the endo- 
thelial cells lining the lymph spaces appear to proliferate, giving rise to 



136 TUMORS. 

a variety of rounded, elongated, or reticular structures, which somewhat 
resemble a typical gland formation. Such tumors are sometimes called 
adenoid sarcomata, but they require more careful and extended study 
before they can be definitely classified. Some of them belong to the 
tumors of the next class. 

ENDOTHELIOMA. 

Under the name of endotheliomata are grouped a number of tumors 
which on the one hand are closely related to the sarcomata in genesis, 
and in some cases in appearance, while on the other hand some of them 
so closely resemble some forms of carcinoma as to be difficult of distinc- 
tion from them. The endotheliomata originate in that form of connec- 
tive-tissue cells called endothelium, and seem to develop by a prolifera- 
tion of these. Sometimes the cells of the endotheliomata resemble 
closely the normal endothelium; sometimes, however, they differ con- 
siderably from them, being occasionally very large, often thick and 




-.'. '■■-- * -■--—_--..--.; -.- ' /■ --.-'I '."'-;v, • .-< -f-.- -*? ■ 




-v 



Fig. 57.— Endothelioma of Dura Mater. 



irregular in shape, and even nearly cylindrical or cuboidal. They are 
associated with a more or less abundant vascular stroma, which may be 
alveolar in formation. In this case, as in alveolar sarcoma, it may often 
be seen that the cells have an intimate relationship to the trabecule of 
the stroma. Sometimes the cells of the endotheliomata are packed to- 
gether in dense concentric masses (Fig. 57), which may have a glistening 
appearance, and such tumors are sometimes called cholesteatomata. 
Although, for the most part, the peculiar glistening appearance of these 
tumors is due to the closely packed thin cells which compose them, they 
not infrequently contain crystals of cholesterin, sometimes in large 
quantities, which may share in producing their characteristic appear- 
ance. But the cholesterin may be absent or present in small amount. 
The endotheliomata may occur of considerable size and be nodular, 



TUMORS. 137 

or they may be multiple, numerous small tumors being scattered over 
the surface of the part in which they grow; they may even form a 
thicker or thinner pellicle over surfaces, or cause adhesions between 
adjacent organs. They may form metastases. They occur in the dura 
mater and pia mater, in the pleura and peritoneum, and have been 
described in the lymph nodes, ovary, liver, brain, and testicle. 1 

LIPOMA. 

Lipomata are tumors formed of fat tissue. The fat tissue occurs in 
lobules and is similar to normal fat, except that the cells and lobules are 
usually larger. There may be little connective tissue in the tumors, 
when they are very soft, almost fluctuating — lipoma molle — or there may 
be so much as to give the tumor considerable firmness— /^ro -lipoma. 
They may be in part transformed into mucous tissue — myxo-lipoma. 
Cartilage not infrequently develops in them, or they may undergo par- 
tial calcification. 

Occasionally the blood-vessels are very abundant and dilated — lipoma 
telangiectoides. They are usually sharply circumscribed, but may infil- 
trate surrounding tissues. They are not infrequently pediculated. They 
sometimes grow to enormous size, and may ulcerate. 

They are usually isolated, but may be multiple. They are the most 
common of tumors, occurring usually in the subcutaneous or other 
fat tissue. They may occur in the mucous membrane of the gastro- 
intestinal canal, in the peritoneum, more rarely in the dura mater, 
kidney, liver, and lungs. They are benign tumors, not forming metasta- 
ses, but they may be deleterious by ulceration or gangrene, and when not 
fully removed may exhibit local recurrence. 

CHONDROMA. 

These tumors, composed of either of the physiological forms of carti- 
lage, are usually hard, but sometimes quite soft. The cells do not pre- 
sent the same uniformity in size, shape, number, and relative position 
that they do in normal cartilage. Sometimes they are very large, 
spheroidal, and grouped in masses, and again small and far apart. They 
are frequently fusiform or branching. Fibrillar connective tissue in vary- 

1 This class of tumors is unsatisfactory, for, as will be seen, we have no very 
definite morphological characteristics which cover all cases, and their relations to 
other tumors are so close that we often need to know the seat of the growth and some- 
thing of its genesis before we can arrive even at a measurably definite determination 
of it, and even then we may fail. This indefinite state of affairs arises from the fact 
that we do not yet know enough about the normal relationships between endothelial 
and other connective-tissue cells; and, furthermore, we do not yet know exactly to 
what extent the progeny of one class of cells may grow to resemble or become iden- 
tical with those of another class. 
11 



138 



TUMORS. 



ing quantity is usually present in the chondromata, either as a capsule, or 
running in bands between the nodules of cartilage, or passing in fascicles 
into them (Fig. 58). The cartilage may change to mucous tissue/ form- 



^gilli ill: ,. 






Q 



mm 




m 



Fig. 58.— Chondroma op Subcutaneous Connective Tissue. 

ing myxo- chondroma (Fig. 59); the cells may undergo fatty degeneration 
or they may calcify or ossify. Ohondromata frequently form a part of 
mixed and complex tumors. 




Fig. 59.— Myxo-Chondroma op Cervical Region. 






They may form in connection with bone or cartilage, and are often 
traceable to irregularities in foetal development. Or they may occur in 
soft parts where cartilage is not normally present, as in the parotid, tes- 

1 This change of one form of tissue into another is called metaplasia, and is not 
uncommon among the members of the connective-tissue group, as well as in the 
tumors which are formed after their types. 



TUMORS. 139 

tide, mamma, and ovaries, where they are apt to be mixed with other 
tissues; or in subcutaneous connective tissue and fasciae. 

They are in general benign tumors, but metastases sometimes occur, 
most frequently in the lungs, sometimes in the heart. 

Small hyperplastic growths on the surfaces of cartilage are called 
ecchondroses. 

OSTEOMA. 

The formation of bone in the body in abnormal places occurs quite 
frequently and under a great variety of conditions. It is on this account 
not easy to define the term osteoma, and it is frequently difficult to 
determine whether or not a given mass of new- formed bone is an osteoma 
or not. Bone tissue often occurs in tumors of the connective-tissue 
group as a secondary or complicating structure — osteo-fibroma, osteo- 
chondroma, osteosarcoma, etc. It may occur in muscles as a result of 
certain exercises, or as a result of a peculiar inflammatory process (see 
Lesions of the Muscles), or it may occur in connection with chronic in- 
flammation in a variety of tissues. A circumscribed mass of abnormal 
bone, not of inflammatory origin, may be called an osteoma. Small 
masses of new-formed bone of various shape, projecting from a bony 
surface and frequently of inflammatory origin, are usually called osteo- 
phytes. Bony tumors projecting from the surface of bones are frequently 
called exostoses. 

An osteoma may be loose in texture, consisting of bone tissue similar 
to cancellous tissue, or it may be denser, resembling compact bone tis- 
sue, or it may be very hard and dense like ivory, so-called ivory exostoses. 
The difference between these forms lies chiefly in the varying number 
and size of the vascular and medullary spaces which they contain. 

Osteomata may develop in connection with the bone or periosteum, 
which is most frequently the case, or, independently of bone, in soft 
parts. 

New-formed bone has been found in the soft parts of the body, in the 
brain substance, dura mater and pia mater; in the pleura, diaphragm, 
and pericardium; in the skin, choroid, air passages, lungs, and penis, 
and in other places. To what extent some of these bone formations may 
have been due to inflammatory action it is not jjossible to say, and it is 
quite probable that the fuller knowledge of the future may show rela- 
tionships between the development of certain tumors and some forms of 
chronic inflammation which we do not now recognize. 

The growth of the osteomata is, as a rule, slow. They are benign 
tumors, and are not infrequently multiple. 

GLIOMA. 

The gliomata are developed in connection with the characteristic 
connective-tissue framework of nerve tissue, the neuroglia, which in 



140 



TUMORS. 



structure many, though usually not all, of its cells closely resemble. 
Small cells with inconspicuous bodies and numerous delicate branching 
processes are most characteristic; but in connection with these there is 
usually a greater or less number of small spheroidal cells with proportion- 
ally large nuclei (Fig. 60). It is usually necessary to shake sections in 





Mite? 

mm 



Fig. 60.— Glioma of Brain. 

water or carefully tease fragments of the tumor in order to see the charac- 
teristic neuroglia or so-called " spider " cells (Fig. 61). These tumors 
may contain very numerous and frequently dilated thin-walled blood- 
vessels. They may be very soft or moderately hard; and especially 
when occurring in the substance of the brain are frequently not 




Fig. 61.— Neuroglia or " Spider " Cells from Glioma of Brain. 
Teased specimen. 

sharply outlined against the adjacent normal tissue. They usually oc- 
cur singly, and are comparatively slow in growth. 

They are very apt to be complicated with other tumor tissue, forming 
glioma-myxoma, glio-sarcoma, etc. Owing to the abundance of thin- 
walled blood-vessels and the softness of the growth, they are liable to in- 
terstitial haemorrhages, and may then, when occurring in the brain, 
readily be mistaken for ordinary apoplectic clots. They are liable to 



TUMORS. 141 

fatty degeneration. They usually occur in the brain, spinal cord, and 
in the optic and other cerebral nerves. The so-called gliomata of the 
retina are usually small spheroidal-celled sarcomata. 

Pure gliomata are benign tumors, though in their most common com- 
bination with sarcoma they may be very malignant. Their usual situa- 
tion, however, is such as to make them almost always significant, 
although technically they are benign tumors. 1 

MYOMA. 

Tumors composed of muscular tissue are of two kinds, following the 
two physiological types of muscle tissue, the non-striated and the 
striated. 

I. Leiomyoma, Myoma-levicelhdare. — The characteristic elements of 
these tumors are fusiform, smooth muscle fibres, with elongated or rod- 
shaped nuclei. These are packed closely together, frequently interlac- 




Fig. 62.— Myoma of Uterus. Leiomyoma. 

ing and running in various directions, and are intermingled with a 
variable quantity of more or less vascular fibrillar connective tissue (Fig. 
G2). When, as is not infrequently the case, the connective-tissue ele- 
ments are present in large amount, the tumor is called fibro-myoma. 
It is not always easy in sections to distinguish between these tumors and 
certain cellular fibromata, but the characteristic shape of the isolated 
cells and their nuclei, together with their uniformity in size, will usu- 
ally suffice. These tumors are frequently infiltrated with lime salts, and, 
owing to their density and lack of blood-vessels, they not infrequently 
degenerate, forming cysts or becoming gangrenous. They may occur 
singly or multiple, are usually of slow growth, may be large or small, 
and are benign. They may occur wherever smooth muscle tissue exists. 

1 Our knowledge of the normal neuroglia is still too meagre to permit us to under- 
stand very thoroughly this class of tumors, and to separate it as precisely as could be 
wished from certain of its allies among the abnormal connective-tissue growths. 



142 TUMORS. 

They are most frequently found in the uterus, where they are often mul- 
tiple. They may occur in the wall of the gastro-intestinal canal, and 
have been seen in the bladder and in the skin of the nipple and scrotum. 
The so-called hypertrophies of the prostate, so frequent in advanced life, 
are usually leiomyomata of the interstitial muscle tissue of that gland. 

II. Myoma strio cellular e or Rhabdomyoma. — In these rare tumors, 
striated muscle fibres are the characteristic elements. They very rarely 
compose a great part of the tumor, but are intermingled with other ele- 
ments, fibrillar connective tissue, spindle-shaped and spheroidal cells of 
various forms, which often appear to be incompletely developed muscle 
cells. They are not infrequently associated with sarcomatous tissue. 
Blood-vessels and sometimes nerves are also present. The muscle fibres 
differ, as a rule, from normal striated muscle fibres in their arrangement, 
which is usually quite irregular, and also in size, being in general smaller 
than normal fibres, although varying greatly. The sarcolemma is either 
absent or incompletely developed. These tumors are usually small or of 
moderate size, and are supposed to originate from inclusions of cells 
destined to form muscle tissue in places where they do not belong. 

In the heart and certain, other muscular parts, small circumscribed 
masses of striated muscle tissue have been described, and are sometimes 
called homologous rhabolomyomata. But genuine heterologous rhabdo- 
myomata are, in almost all cases thus far recorded, confined to the geni- 
to-urinary organs, kidney, ovary, and testicles. The writer (T. M. P.) 
has described an exceptional case of rhabdomyoma occurring in the 
parotid gland. 1 These tumors, when not associated with other and 
malignant tumors, are benign, and are of much greater theoretical than 
practical interest. • 

NEUROMA. 

A true neuroma is a tumor containing new-formed nerve tissue. Such 
tumors are comparatively rare. Tumors developed in the connective 
tissue of nerves and composed usually of fibrous or mucous tissue are 
common, and are frequently called neuromata, but they should be called 
fibromata ormyomata, etc., of the nerves, or false neuromata. The true 
neuromata are of two kinds, ganglionic or cellular neuromata and 
fibrillar neuromata, depending upon the character of nerve tissue which 
they contain. The ganglionic neuromata are found associated with 
other structures in certain of the teratomata in the ovaries, testicles, and 
in the sacral region; they also occur in the gray matter of the brain. 

The fibrillar neuromata are, according to Virchow, of two kinds, 
myelinic and amyelinic, depending upon whether the nerve fibres which 
they contain are medullated or not. The neuroma myelinicum is the 

1 American Journal of the Medical Sciences, April, 1883. 



TUMOfJS. 



143 



more common and the best understood. The medullated nerve fibres 
in these tumors are associated with fibrillar connective tissue, and are 
usually curled and intertwined in a most intricate manner. They occur 
either singly or multiple on the peripheral nerves. They may oc- 
cur in considerable numbers as nodular tumors on the branches of a 
single nerve trunk, or they may form an irregular, diffuse, nodulated 
enlargement of the nerve branches — plexiform neuroma. These neu- 
romata may or may not be painful. They not infrequently form at the 
cut ends of the nerves in amputation stumps. They are benign tumors, 
never forming metastases. 

The false neuromata (Fig. 63) are myxomata, or fibromata, or 










Fig. 63.— Fibroma (False Neuroma) of Lumbar Nerve. 
The fibrous tissue is loose in texture and in places cedematous, so that it considerably resembles 
mucous tissue. 

sometimes myxo-sarcomata of the nerve sheaths or intrafascicular con- 
nective tissue, and may occur singly or multiple. In the latter case, they 
may affect the branches of a single nerve trunk, or they may be found 
on nearly all the cerebro-spinal peripheral nerves. The writer (T. M. P.) 
has described a case (Fig. 64) in which over eleven hundred and eighty- 
two distinct tumors were found distributed over nearly all the peripheral 
nerves of the body. 1 The nerve fibres in these tumors may be crowded 
apart by the new growth and considerably atrophied; or, in cases in 

1 American Journal of the Medical Sciences, July, 1880 



144 



TUMORS. 



which the tumor is composed of soft tissue, as in myxoma or the soft 
fibroma, they may pass through or around the tumor entirely unchang- 
ed. The multiple false neuromata are in many cases congenital. 




Fig. 64.— Multiple Fibromata (False Neuromata) op Pneumogastric Nerve. 

natural size. 



One-quarter 



ANGIOMA. 

Angiomata are tumors consisting in large part or entirely of new- 
formed blood-vessels or blood-cavi ties. In many tumors of various kinds, 
the new-formed or the old blood-vessels may be very abundant or prom- 
inent by reason of their dilatations; the blood-vessels of otherwise normal 
tissues may also be largely dilated, thus simulating vascular tumors. 
These are, however, not true angiomata, although sometimes reckoned 
among them, and in many cases closely allied to them. Such are the so- 




Fig. 65.— Angioma telangiectoides (Vascular Nevus) from Skin over Scapula of Child. 



called arterial varix, or cirsoid aneurisms, and haemorrhoids. True 
angiomata are of two kinds: 

I. Those formed largely of capillary blood-vessels with either thin or 
thickened walls, imbedded in a more or less abundant connective-tissue 
stroma. These are called simple angiomata or angioma telangiectoides. 
The walls of the vessels in these tumors are frequently dilated or pouched, 
and usually form a tangle of curled and intertwined vessels. They occur 



TTTMORS. 



U5 



most frequently in the skin or subcutaneous tissues (Fig. 65), usually 
about the face, and may project above the general surface or be on a 
level with it. Such are the so-called vascular nwvi or strawberry marks, 
which are usually congenital. They are sometimes sharply circum- 
scribed, and sometimes merge imperceptibly into the surrounding skin. 
They sometimes occur in the mucous membranes, in the mamma, bones, 
and brain. They are benign tumors, never forming metastases, but may 
be associated with sarcomata. 

II. The second form of angioma, called angioma cavernosa, consists 
largely of a series of intercommunicating, irregular-shaped larger and 
smaller blood-spaces lined with endothelium, and surrounded by a vari- 
able quantity of fibrillar connective tissue, which may contain smooth 
muscle cells (Fig. 66). They resemble the erectile tissue of the cor- 
pora cavernosa of the penis and clitoris. They are apparently formed 







Fig. 66.— Angioma cavernosa of Liver. 

by a dilatation of old and new-formed capillaries and veins. They are 
sometimes erectile and sometimes pulsating, and are not infrequently 
multiple. They may be seated in the skin and subcutaneous tissue, 
forming the so-called projecting naevi, or in internal organs. They are 
often found in the liver and less frequently in bone, the brain, spleen, 
uterus, kidney, intestines, bladder, and muscles. They are usually of 
little significance, though they may give rise to haemorrhages. 



LYMPHANGIOMA. 

These tumors consist of dilated lymph channels, which either pre- 
serve approximately the general shape of the original lymph vessels, or 
are distinctly cavernous in character, or even cystic (Fig. 67). They 
probably originate in part in new-formed, in part in old lymph channels. 
A strict distinction between tumors formed by a dilatation of preformed 



146 



TUMORS. 



and new-formed lymph channels is not possible, owing to the very prim- 
itive character of some of the ultimate lymph spaces and our lack of 
knowledge of their exact relations to adjacent parts. 

In the lymphangiomata, there may be much or little connective tis- 
sue between the dilated channels, which are usually filled with a trans- 
lucent or milky fluid resembling, and probably identical with, the normal 
lymph. These tumors are usually congenital, but are sometimes ac- 
quired. They usually occur in the skin as soft, sometimes considerably, 
sometimes but slightly elevated tumors, and may occur in the tongue— 




Fig. 67.— Congenital Lymphangioma from Arm of Child. 

some forms of so-called macroglossia. They are benign tumors, but 
may rupture, giving rise to a serious lymphorrhoea. 



TUMORS IN" WHICH EPITHELIAL CELLS ARE PREDOMINANT OR CHARAC- 
TERISTIC ELEMENTS— EPITHELIAL TUMORS. 

I. Adenoma. 

II. Carcinoma. 

General Considerations. — The tumors thus far described in detail, 
with the exception of the gliomata, are formed on the type of tissues 
which develop from the parablast. The epithelial tumors, on the other 
hand, originate in one or other of the layers of the archiblast, and we 
have accordingly two series of criteria by which to describe and identify 
them: first, morphological, and, second, histogenetic criteria. 

While in the main, in the normal body, the general distinctions 
between epithelial and other tissues are fairly well marked, there are 
still particular cases, especially those in which epithelial tissues are in 
process of physiological growth or rejuvenation, in which the distinc- 
tions are quite ill-defined. When we remember the rapid growth of 
many tumors, the tendency to incomplete formation of their cells, their 



TUMORS. 147 

diverse seats, and the various complicating conditions under which they 
originate and develop, it does not seem strange that the exact limitations 
of this class of tumors are not easy to fix, nor that they seem sometimes 
to merge into one another and into tumor tissues belonging to other 
classes. If epithelial cells, under all circumstances, had a definite and 
characteristic structure, or if, on the other hand, we could always know 
whether a given cell group originated in epithelium or not, the matter 
of distinguishing between tumors of this and other classes would be sim- 
ple and easy enough. As it is, in some cases both morphological and 
histogenetic criteria fail us, and the clinical history and gross appear- 
ance are not characteristic. Such cases, which are indeed rare, but 
which do sometimes occur, suggest to us the possibility that the desira- 
bility of accurate classification has led us into seeking distinctions which 
Nature herself has not sharply drawn. While these difficulties in special 
cases must be acknowledged, the distinctions are in the main definite 
enough, and very useful both for clinical and scientific purposes. 

Epithelial tumors always contain, in addition to the more or less 
characteristic cellular elements, a connective-tissue stroma which gives 
them support and carries the vessels. This stroma may be sparse or 
abundant, may contain few or many cells, is sometimes arranged in ir- 
regular fascicles or bands, and very frequently forms the walls of well- 
defined, variously shaped spaces or cavities called alveoli, in which the 
epithelial cells lie. The epithelial cells, in most cases, lie along the walls 
of the alveoli without an intimate connection with them, as is the case 
in the alveolar sarcomata. They are, moreover, packed together without 
more intercellular substance than the usual cementing material common 
to epithelial cell masses. In this lack of fibrillar intercellular substance 
within the alveoli, and in the loose relationship between the cells and 
the alveolar walls, lie in many cases the chief morphological distinctions 
between certain carcinomata and alveolar sarcomata. 

In certain of the epithelial tumors, there is a reproduction of typical 
gland tissue of various kinds, depending upon the seat and conditions of 
growth of the tumor. Such tumors are called adenomata. A simple 
hypertrophy of a gland, or an increase in its size by excessive growth of 
its interstitial tissue, do not constitute an adenoma. There must be an 
actual new formation of more or less typical gland tissue. This is not 
always or frequently of exactly the same character as the gland tissue in 
which it originates, and always exhibits a certain lack of conformity to 
the type in structure and mode of growth. The alveoli and ducts usu- 
ally have a lumen and sometimes a membrana propria, but the cells may 
differ in shape from one another and from those of the gland from which 
they spring. 

Epithelial tumors in which there is no close conformity to a glandular 
type, but a lawless growth of various kinds of more or less typical epi- 



148 TUMOKS. 

thelial cells in the meshes of an old or new-formed connective-tissue 
stroma, are called carcinomata. 

It will readily be seen that there must be a border region between the 
adenomata and carcinomata where conformity to the glandular type 
merges into the lawlessness of growth characteristic of carcinomata. In 
this border region, a certain degree of individual bias must be permitted 
in assigning a name to the new growth. In some cases a sharp distinc- 
tion cannot be made, or the tumor may share in the characteristics of 
both, and then we very properly make use of the term adeno-carcinoma 
or carcino-adenoma. 

I. ADENOMA. 

The structure of the cellular elements of these tumors and their 
arrangement into acini and ducts vary even more than do those of the 



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Fig. 68.— Adenoma of Mamma. 

normal glands whose types they follow. The acini usually possess a more 
or less well denned lumen and membrana propria (see Fig. 68). The 
adenomata sometimes merge into the surrounding tissue, or are con- 
tinuous with the gland tissue in which they originate; sometimes they 
are distinct in outline and incapsulated. The interstitial tissue is some- 
times abundant, sometimes sparse, and may contain few or many cells. 
The irregularities of their growth often lead to the stoppage of the 
lumina of their ducts and the formation of cysts. They may undergo 
mucous metamorphosis, and may become sarcomatous. 

Adenomata occur in the mamma, ovary, liver, kidney, thyroid, sali- 



TUMORS. 



149 



vary, and lachrymal glands, and in the caruncle; in the mucous mem- 
brane of the nose, pharynx, stomach, intestine, and uterus; and occa- 
sionally in the sebaceous and sweat glands of the skin. The so called 
multilocular cysfcomata of the ovary are among the most important of 
the adenomata. There are numerous papillary and polypoid growths, 
in gland ducts and on mucous membranes, in which there is an actual 
new formation of gland epithelium, but this is usually secondary to a 
primary growth, beneath the epithelial layer, of some other tissue, such 
as fibrous or mucous tissue, and the new growth of gland epithelium 
simply keeps pace with the growth of the latter, to which it serves as an 
investment. Such growths are sometimes classed among the adenomata, 
but do not, strictly speaking, belong there. 




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Fig. 69.— Adenoma of Stomach. 
A form which is on the border-line of carcinoma. 



The adenomata are in general benign tumors, being slow of growth 
and localized, but there are very important exceptions. Some of the 
adenomata of the stomach and intestines belong to the most malignant 
of tumors in rapidity of local extension, in the formation of metastases, 
and the development of cachexia. Certain of the adenomata of the 
mamma and thyroid are also very malignant. It should be remarked, 
however, that, as a rule, the malignant adenomata are those which, in 
structure, lie close upon the border-line between tumors of this class and 
carcinomata (see Fig. 69), and by such observers as incline to lay more 
stress upon clinical than morphological distinctions they are usually 
classed among the latter. 



150 TUMORS. 



CARCINOMA. 



These tumors are composed, as above stated, of a connective-tissue 
stroma, forming more or less well-defined communicating spaces or alve- 
oli, in which lie variously shaped epithelial cells arranged in an atypical 
manner. The stroma, containing few or many cells, may be, especially 
in the advancing portions of the tumor, composed largely of the old con- 
nective tissue of the part. It may, however, be entirely new formed. 
The cells which lie in the spaces or alveoli bear sometimes a very close, 
sometimes but a very general resemblance to epithelium. 

It was formerly believed that new epithelium might be formed, both 
from old epithelial cells and from the connective-tissue cells, and possi- 
bly from white blood-cells, and among many observers this belief still 
exists and has never been disproved. Still, within the last twenty years,, 
the opinion that new epithelial cells in tumors arise exclusively from old 
epithelium has found general acceptance, and for very good reasons. 
No one has actually seen an epithelial cell originate under the micro- 
scope, and until this can be done our beliefs must rest upon indirect 
observations. In the first place, all the epithelial structures in the em- 
bryo originate in the archiblastic layers, that is, in those layers which are 
largely characterized by the presence of epithelium (see page 121). In re- 
generation, after an injury in the adult, a study of the successive phases, 
of the process shows that new epithelium is always formed in continuity 
with the old, and apparently by a proliferation of old epithelial cells. 
Epithelial tumors are almost exclusively found in parts normally contain- 
ing epithelium, and frequently the new growth can be distinctly seen to 
be continuous with the old cells. 

The occurrence of primary epithelial tumors in parts of the body in 
which epithelium does not normally occur, as in bone and the lymph 
nodes, has been recorded, but these [may have been metastatic tumors, 
in which the primary tumor was small and overlooked, or they may have 
.been displaced embryonic germs, which, according to Oohnheim's hypo- 
thesis (see page 11 9), would explain their heterologous occurrence. These 
possibilities of error should be taken into the account in the apparently 
exceptional cases, and it is to be remarked that these are becoming less 
and less as our knowledge increases and our technical facilities for re- 
search improve. 

A considerable number of the tumors formerly described as heterol- 
ogous primary carcinomata are now known to be formed by proliferation 
of endothelium, and hence to belong to another class, although closely 
resembling the carcinomata in structure. 

The occurrence of primary carcinoma of the peritoneum, pleura, and 
pericardium, which is not infrequent, was for a long time inexplicable, be- 
cause it was, and to a large extent still is, believed that the flat cells lin- 



TUMORS. 



151 



ing these great body cavities are true endothelium, and closely related in 
origin, as they are in structure, to the genuine endothelium of the blood 
and lymph vessels, etc. 

But recent embryological researches have shown that this belief is 
not well founded. It was formerly thought that the great serous cavi- 
ties were large lymph vessels formed by the splitting apart of the con- 
nective-tissue layers of the mesoblast. But we now know that the great 
primitive body cavity, which after a time becomes divided into the 
pleural, pericardial, and peritoneal sacs, is originally an outgrowth from 
the alimentary canal. The epithelium of the alimentary canal, how- 
ever, is of archiblastic origin (see page 121), while the connective tissue, 
blood and lymph vessels are developed later from the parablast. Gene- 
tically, therefore, the so-called endothelial cells lining the pleural, peri- 
cardial, and peritoneal cavities are of archiblastic origin and belong 
among the epithelium. Thus a fuller knowledge of the histogenesis of 
the cells lining the great body cavities has shown us that the occurrence 
of primary carcinoma in these cavities is not only not in contradiction 
with the principle of the epithelial origin of carcinoma, but strongly 
confirmatory of it. 

A great practical difficulty in the description, and to beginners, in 
the recognition of the carcinomata and their varieties, lies in the great 
diversity in shape which their cells present. It should be always borne 
in mind that the shape of cells depends in part upon their inherited 
tendencies in growth, which we cannot see under the microscope, but to 
a greater degree upon the varying conditions of nutriment and pressure 
to which they are exposed during life. In the normal body, these con- 
ditions conform to a certain standard, so that cells of a given kind at a 
given stage of development are approximately similar. 

In tumors, however, the lawlessness and lack of fixed conditions in 
growth are such that we may have many young and atypical so-called 
indifferent forms of cells; while even the adult forms may depart widely 
from normal shapes. Thus, in cylindrical-celled carcinomata there are 
many fully developed cells which are never cylindrical; there are many 
others not fully developed which are quite indifferent in form, looking 
just like many other young cells — cells which are not, but which are des- 
tined to become, epithelium. Finally, we have the cells produced by 
ordinary inflammatory processes about and within the tumor, which 
acts like an irritating foreign body. Thus it is that there is no charac- 
teristic cancer cell, as was formerly supposed. Some of them are typi- 
cal and some not, and the more typical ones may look just like normal 
epithelial cells, and the atypical ones just like simple inflammatory 
cells, or young connective-tissue cells, or white blood-cells. It is always 
in the topography, together with the general characters of the cells and 



152 



TUMORS. 



the situation of the growth, that we must seek for the evidences of its 
nature. 

The carcinomata are very prone to local extension, the advancing 
tumor cells in the periphery making their way through the lymph 
spaces and forming new foci (Fig. 70). Metastasis is of frequent occur- 
rence in some forms, and takes place chiefly, though not exclusively, 
through the lymph vessels, frequently involving adjacent or remote 
lymph nodes. The growth of the tumor cells in the lymph vessels, 
either in the immediate vicinity of the original tumor or following 
metastasis in a distant part of the body, may cause these to become dis- 




Fig. 70.— Cancer Cells infiltrating the Tissue in the Vicinity of a Tumor. 
From carcinoma mammae. 



tended, and, on free surfaces like the pleura and peritoneum, to form 
a whitish, elevated network. Transverse sections of such distended 
lymph vessels are shown in Fig. 71. The secondary tumors are in the 
main similar in general structure to the primary foci, but may vary 
from them in vascularity and the abundance of the stroma, or in the 
shape of the cells. The carcinomata are, as a rule, malignant tumors, 
but the different forms vary much in this respect. They are liable to 
fatty, colloid, mucous, and amyloid degeneration, and are especially 
prone to ulceration, to haemorrhage, and simple inflammation (Fig. 72). 



TUMORS. 



153 



They may become partially calcified, and are not infrequently combined 
with other forms of tissue in the mixed tumors. 

They are more frequent in middle and old age than in the young, 
but they may occur at any age. 






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Fig. 71.— Metastatic Carcinoma in Lymph Vessels of the Pleura. 
The primary tumor was in the liver. 

Forms of Carcinoma. — In certain cases of carcinoma which occur in 
the skin and in some mucous membranes, the cells present the structure 
and general characters of the epithelium of the part in which they 



All 




Fig. 72.— Carcinoma Uteri. 
Showing accumulation of pus cells between the epithelial cells of the tumor. 

occur; and since here the tendency of the cells as they approach the 
surface is to become flattened or squamous, these tumors are called 
squamous or flat-celled carcinomata, or simply Epitheliomata. 

In another class of tumors, such as frequently occur in the gastro- 
12 



154 TUMORS. 

intestinal canal and uterus, the cells are more or less cylindrical in 
shape, forming a palisade-like lining to the irregular alveoli; such tumors 
are called Cylindrical-celled Carcinomata, although here again many of 
the cells are not cylindrical at all, but may have a great variety of 
forms. 

There is a third and very common form of tumor, in which the epi- 
thelial cells have no constant characteristic shape, but vary as much as 
do the cell forms in the various glands of the body. Such tumors are 
conveniently classed together as gland-celled carcinoma, or Carcinoma 
simplex. 

In addition to these forms, there are several others which depend for 






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\M •• -'■ &>*■: ■■■■■ ,"- ;-- ';■-■;■■*> \ •■■.■ /- . ' l£j 

Fig. 73. — Epithelioma of the Neck. 
J Shows epithelial pearls, spined cells, and reticular masses of variously shaped epithelial cells. 

their characteristics upon various metamorphoses or degenerations, or 
upon the preponderance of one or other of the anatomical constituents 
of the growth. It will be most convenient to give a brief description of 
these various kinds, one after another, with the understanding that they 
are not absolute specific forms, but are simply varieties which it is con- 
venient to recognize for clinical as well as anatomical purposes. 

Flat-celled Carcinoma, or Epithelioma.— -These tumors occur in the 
skin and in the mucous membranes, which are covered with squamous 
epithelium. The cells present all of the various forms which normally 
exist in these parts — the cuboidal and polyhedral cells of the rete Mal- 
pighii, as well as the more superficial flattened forms (Fig. 73). Fre- 



TUMORS. 



155 



quently the spined cells, or so-called " prickle cells," are largely repro- 
duced. Having to a certain extent the same life history as the cells in 




Fig. 74.— Epithelioma of Axillary Lymph Node. 
This metastatic tumor was secondary to a large epithelioma of the back of the hand, Fig. 75. 
The small cells with darker nuclei are the cells of the lymph node. 

which they originate, many of the tumor cells become dry, thin, and 
horny, like the epidermis cells, as they grow older; and since their 





Fig. 75.— Epithelioma of Back of Hand. 
The flat tumor occupied nearly the entire back of the hand, and was ulcerating at the centre. 
The figure shows the edge of the tumor and a portion of the ulcer. The papillae of the skin over 
the edge of the growth are hypertrophied, and the tissue about infiltrated with small spheroidal 
cells. 

growth and changes often occur within the old lymph spaces of the 
affected tissue, or in the new-formed alveoli, the cells are sometimes 



156 TUMORS. 

packed together in spheroidal, concentric masses called "epithelial 
pearls/' which may sometimes be seen with the naked eye upon or near 
the surface of the growth (Fig. 74). The new cell masses may be large 
or small, may be separated by much or little stroma; often form reticu- 
lar masses, and may infiltrate the tissues deeply or remain near the 
surface; or may project aboye the surface, forming wart-like or papillary 
growths. These tumors frequently ulcerate on the surface, and the skin 
about them is apt to become thickened (see Fig. 75). 

They are most apt to occur in the skin, especially in those parts in 
which it becomes continuous with mucous membranes — lips, external 








Fig. 76.— A Small Epithelioma of the Side op the Nose, X 80. 

nasal openings, eyelids, labia, and glans penis — and are frequent in the 
mouth, oesophagus, vagina, and about the cervix uteri. 

There are also carcinomata of the skin, composed of cuboidal cells 
arranged in tubules or masses, which do not follow the type of the epi- 
thelium of the skin, but rather that of the sweat glands or sebaceous 
glands. These tumors are found most frequently on the nose and eye- 
lids (Figs. 76 and 77). 

Epitheliomata are apt to recur if not thoroughly removed, and may 
form metastases, but in general they are the least malignant of the car- 
cinomata. The prognosis is in most cases good if there is early and 
complete removal. 

Cylindrical-celled Carcinoma. — These tumors, closely allied to some 



TUMORS. 157 

forms of adenoma, occur in the stomach, intestines, and uterus (see 
Fig. 69). The cells may be only in part cylindrical, the remainder 
having various shapes, and all being loosely or closely packed in larger 
or smaller alveoli. They may have much or little stroma. They merge 
imperceptibly into the next class: 

Gland-celled Carcinoma, or Carcinoma simplex. — These, which are 
by far the most frequent of the carcinomata of internal parts, are char- 
acterized by the alveolar structure and by the absence of any special 
characteristic shape in the cells, which may be spheroidal, polyhedral, 
fusiform, or cuboidal. They may or may not resemble the epithelium 







Fig. 77.— Epithelioma of Nose, x 550. 
A portion of the tumor shown in Fig. 76 more highly magnified. 

of the gland in which they originate. They are usually nodular tumors, 
and may be hard or soft. If the stroma is abundant and dense, and 
preponderates over the cellular elements, the tumor is usually hard and 
is called scirrhus or fibro carcinoma (Fig. 78). If, on the other hand, 
the cellular elements largely preponderate, the tumor is usually soft, and, 
if it do not contain too many blood-vessels, may have a general resem- 
blance to brain tissue, and is then called encephaloid or medullary can- 
cer ; or, better, Carcinoma molle (Fig. 79). These are among the most 
malignant of the cancers. The intercellular tissue may become so 
abundant as to nearly obliterate the cellular elements, but it is doubtful 
if carcinoma ever undergoes spontaneous cure in this way. These 



158 



TUMORS. 




Fig. 78.— Carcinoma Mamule. (Scirrhus variety.) 







Fig. 79.— Medullary Carcinoma of Stomach. (Carcinoma molle.) 



TUMORS. 



159 



tumors may be hard in one portion and soft in another. They may 
contain very many blood-vessels, C. telangiectoides. They occur as 
primary tumors in the mamma, liver, thyroid, salivary, and prostate 
glands, in the pancreas, kidney, testicle, and ovary. 

Colloid Carcinoma. — The cells of certain cancers, especially of the 
gastro-intestinal canal, may suffer a more or less complete infiltration 
with a translucent material somewhat resembling gelatin, and called col- 
loid, whose nature is not well understood. Sometimes this infiltration 
is only partial, when the protoplasm of the cells may be more or less 
incroached upon by the translucent droplets of the colloid material; but 
in other cases over large areas the cells are partially or entirely de- 
stroyed, and replaced by the new material, so that the alveoli of the 




Fig. 80.— Colloid Carcinoma of Rectum. 



tumor are distended by it, and their walls appear very distinct in the 
midst of the colloid substance (Fig. 80). In such cases, the alveolar 
structure of the tumor is sometimes very evident to the naked eye, and 
these tumors are therefore often called alveolar carcinoma. Sometimes 
only a part of the tumor is affected in this way. 

Carcinoma myxomatodes. — The cellular elements of carcinomata may 
suffer mucous softening, and thus larger and smaller cysts containing a 
mucous fluid are sometimes formed. To this form of metamorphosed 
tumor the above name is sometimes applied, but it more properly belongs 
to cancers in which the stroma is composed of mucous tissue (Fig. 81). 
Such tumors are most frequently found in the gastro-intestinal canal 
and mamma. 



160 



TUMORS. 



Melano- Carcinoma. — Tumors of this class are rare, and are character- 
ized by the presence of a variable quantity of black or brown pigment 












Fig. 81.— Carcinoma Myxomatoses Mammje. 



particles either in the stroma or the cells. They are usually soft and 
malignant, and most frequently occur in the skin. 1 



1 Bibliography. — The most extensive and important work on tumors, containing a 
vast store of information, is that of Rudolph Virchow, "Die krankhafte Geschwulste." 
It is not completed, and is somewhat old, but is still invaluable as a work of refer- 
ence. The section on tumors in v. Pitha and Billroth's work on surgery (" Handbuch 
der allgemeinen u. speciellen Chirurgie "), which comprises the first section of the 
second volume, by Dr. Lucke, is very complete. A valuable bibliography and digest 
of recent observations on tumors will be found in the last edition of Birch-Hirschf eld's 
work on pathological anatomy (" Lehrbuch der pathologischen Anatomie"), vol. i. ; 
also in Ziegler's " Lehrbuch der path. Anat.," Band i., 5th ed., 1887. 



PART III. 



MOEBID ANATOMY OF THE OEGANS. 



THE NERVOUS SYSTEM. 



THE MEMBRANES OF THE BRAIN. 
THE DUEA MATER. 

The dura mater is a dense connective-tissue membrane, which serves 
the double purpose of a periosteum for the inner surface of the cranial 
bones, and of an investing membrane for the brain. It is itself but 
poorly supplied with blood-vessels, but it contains the large venous si- 
nuses which carry the blood from the brain. Lesions of the dura mater, 
therefore, are apt to be associated with lesions of the cranial bones, of 
the pia mater, or of the venous sinuses. 

In young children the dura mater adheres closely to the inner sur- 
face of the cranial bones, in adults it is more readily detached, and in 
old persons it is again more adherent. Chronic inflammation of the 
external layers of the dura mater also renders it more adherent to the 
bones. 

Haemorrhages. — We find extravasations of blood between the dura 
mater and the cranial bones, in the substance of the membrane, and 
between the dura mater and the pia mater. 

The haemorrhages in the substance of the dura mater are usually 
small and of little consequence. 

The haemorrhages between the dura mater and the pia mater occur 
with chronic pachymeningitis, or are derived from the vessels of the 
pia mater. 

The haemorrhages between the dura mater and the cranial bones are 
produced by blows and injuries of the head. They are often of consid- 
erable size, separate the membrane from the bones, and may compress 
the brain. They are often associated with laceration of the brain, and 
haemorrhages between the dura mater and pia mater. 

The pressure on the head of the infant in labor may produce, in ad- 
dition to the extravasations of blood between the bones and the pericra- 
nium, additional extravasation between the bones and the dura mater. 

Thrombosis of the venous sinuses is not uncommon. Any inflamma- 
tion of the dura mater is liable to produce it; injuries and inflammations 



164 THE NERVOUS SYSTEM. 

of the brain and pia mater, of the cranial bones, of the middle ear, and 
of the scalp, may also produce thrombosis. The changes in the blood 
produced by the exhausting and infectious diseases may produce throm- 
bosis of the venous sinuses, as they do of the veins in other parts of the 
body. There are also rare cases in which such a thrombosis is devel- 
oped without discoverable cause in persons previously healthy, and pro- 
duces marked symptoms and death. 

Some of these thrombi are firm, of white or red color, and apparently 
produce no secondary lesions. 

Others are of firm consistence, but they produce softening with 
small haemorrhages of portions of the brain. In these cases, the throm- 
bus extends from the venous sinus into one of its veins, and the portion 
of brain belonging to this vein is softened and hemorrhagic. Such a 
softening of the brain is often attended with inflammation of the pia 
mater. 

In other cases, the thrombi are soft and puriform; fragments of them 
become detached and lodge as infectious emboli in the arteries in differ- 
ent parts of the body. 

Inflammation of the dura mater is called pachymeningitis, and this 
may involve the external layers of the membrane, 'pachymeningitis ex- 
terna, or the internal layers, pachymeningitis interna. It may further- 
more be either acute or chronic. The tissues of the substance of the 
dura mater participate to a greater or less degree in these changes, but 
the chief lesions are upon the surfaces. 

Acute pachymeningitis externa is usually secondary to injuries or 
diseases of the cranial bones; thus fractures of the skull, either depressed 
or not, ostitis, caries, suppurative inflammation of the internal and 
middle ear and mastoid cells, may produce it. The dura mater is usually 
congested, thickened, and softened, and may present small ecchymoses. 
The inflammation is usually suppurative, and pus may accumulate be- 
tween the membrane and the bone, or in the substance of the membrane. 
The areas of inflammation are not usually extensive. It sometimes in- 
duces thrombosis of the venous sinuses, and sometimes gangrene of the 
dura mater occurs. The inflammation may extend to the inner surface 
of the dura mater, to the pia mater and brain, or it may remain localized 
and undergo resolution. 

Acute pachymeningitis interna may be secondary to inflammation of 
the external surface, or it may occur as a complication in pyaemia, puer- 
peral fever, chronic diffuse nephritis, in the exanthemata and erysipelas, 
or idiopathically. There is a general or circumscribed production of 
fibrin and pus, so that the internal surface of the membrane is lined 
with a layer of soft, yellow exudation. 

Simple chronic pachymeningitis consists in the formation of new 
connective tissue in the dura mater, by which it becomes thicker, and 



THE NEBVOUS SYSTEM. 



165 



in many cases abnormally adherent to the bones of the skull. This 
thickening may be general or circumscribed, and may involve the entire 
thickness of the membrane. Not infrequently, when the external layers 
are especially involved, firm adhesions to the skull occur, with ossification 
of the outer layers, so that shreds of the membrane containing little 
masses of bone (osteophytes) remain sticking to the skull when the mem- 
brane is stripped off. 

There is an important form of chronic inflammation of the internal 
layer of the dura mater, called pachymeningitis interna ftcemorrhagica, 
characterized by the formation of layers of new delicate connective tis- 
sue with numerous verv thin-walled blood-vessels from which the blood 




Fig. 82.— Chrontc Pachymeningitis interna hemorrhagica. 



is prone to escape. The membrane may at first appear as a delicate 
fibrinous pellicle, with small red spots scattered through it, or it may 
look like a simple reddish or brown staining of the inner surface of the 
dura mater. Microscopical examination shows this membrane to consist 
of numerous blood-vessels, mostly capillaries with very thin walls, which 
maybe distended or pouched, and which have grown out from the vessels 
of the dura mater (Fig. 82). Between the vessels is a homogeneous or 
slightly differentiated basement substance, containing a variable number 
of spheroidal, fusiform, or branching cells. Eed blood-cells in variable 
quantity, and blood pigment in various forms, frequently inclosed in the 



166 THE NERVOUS SYSTEM. 

new cells, and small calcareous concretions (brain sand) (Fig. 83), also lie 
in the intervascular spaces. In more advanced stages, the new mem- 
brane may become greatly thickened, its outermost layers being changed 
into dense fibrous tissue with obliteration of the vessels; while the more 
recently formed layers are similar in structure to those at first developed. 
Considerable blood usually escapes from the vessels of the new membrane 
by diapedesis, in all stages of its formation, and the vessels are also very 
liable to rupture, giving rise to extensive haemorrhages either into the 
substance of the membrane or between it and the pia mater. Sometimes 
masses of new tissue and blood, from half an inch to an inch or more in 
thickness, are in this way formed, greatly compressing the brain. These 
new membranes are most frequently formed over the convexity of the 
brain, but may extend over nearly the entire surface of the dura mater. 
Sometimes, when old, the entire membrane, densely pigmented and firm, 
lies loosely beneath the dura mater without compressing the brain or 
giving any clinical indication of its presence. The membrane may in- 




Fig. 83.— Brain Sand from Pachymeningitis interna. 

duce chronic changes in the pia mater, with or without accompanying 
changes in the cortical portion of the brain. 

Earely, serum accumulates between the layers of the new membrane, 
and in this way cysts of large size may be formed. In rare cases, diffuse 
suppuration of the entire new membrane occurs. 

The slighter degrees of this form of inflammation may occasion no 
^symptoms during life. They are not infrequently found in persons 
suffering from various chronic brain lesions and from chronic alcoholism, 
but they may occur unassociated with complicating lesions. The more 
advanced forms of the lesion are frequently found in idiots, epileptics, 
etc. 

Tubercular pachymeningitis may occur secondarily to that form of 
inflammation in the pia mater or the bones, or as a part of general 
miliary tuberculosis. The tubercles may be situated on either surface of 
the membrane or in its substance, and may be single or aggregated, form- 
ing large masses. 

Syphilitic pachymeningitis manifests itself by the formation of 
so-called gummy tumors either upon the external or internal surface of 
the dura mater. These tumors may be single or multiple, and vary 



THE NERVOUS SYSTEM. 167 

greatly in size. They may be accompanied by simple inflammatory 
changes in the dura mater in their vicinity. They may undergo suppu- 
ration with the formation of abscess; the inflammation may extend to 
the pia mater, inducing simple or syphilitic meningitis and adhesions 
between the dura mater and pia mater. The gummata may, on the 
other hand, when occurring on the outer surface of the membrane, cause 
absorption and perforation of the bones of the skull. 

Tumors. — The most common tumors of the dura mater are sarcomata, 
and of these the spindle-celled forms are of more, the round and poly- 
hedral celled of less frequent occurrence. They may grow from either 
surface of the membrane. Some of the round and polyhedral celled 
forms are soft and very vascular, and are apt to involve the neighboring 
pia mater and brain tissue, or the bones of the skull, which they may 
perforate. They sometimes project through the opening in the skull 
in fungous, bleeding masses. 

Psammomata are small, globular tumors, often multiple and pedicu- 
lated, growing from the inner surface of the dura mater. They are 
usually composed of tissue sarcomatous in character, and contain 
variously shaped calcareous concretions similar in appearance to the so- 
called brain sand. 

Endotheliomata. — These tumors may grow inward or outward, causing 
pressure on the brain or absorption and perforation of the bones; they 
often attain considerable size. Some of these tumors somewhat resemble 
certain forms of epitheliomata (see Fig. 57), and have often been described 
as primary carcinomata. 

Fibromata and Lipomata occur rarely in the dura mater and are of 
small size. 

Small Chondromata are sometimes found connected with the dura 
mater at the base of the brain. 

Osteomata. — In addition to the formation of osteophytes in chronic 
external pachymeningitis, plates, and, more rarely, globular masses of 
bone may be formed in the dura mater, unconnected with the bones of 
the skull. They are most frequently found in the falx cerebri, but may 
occur elsewhere. The new bone may be dense or loose in texture, and 
usually produces no symptoms. 

THE PIA MATER. 

The external surface of the brain is invested by a connective-tissue 
membrane which covers the convolutions, dips down into the sulci, and 
extends into the ventricles. This membrane is abundantly supplied with 
blood-vessels, and from it numerous vessels extend into the brain, so that 
any disturbance in the circulation of the blood in the pia mater involves 
a disturbance in the circulation of the blood in the brain also. 



168 THE NERVOUS SYSTEM. 

The connective tissue which makes up the pia mater is arranged in a 
series of membranes and fibres reinforced by elastic tissue, so arranged 
as to form a spongy membrane containing numerous cavities more or 
less filled with fluid. These cavities are continuous with the perivascu- 
lar spaces which surround the vessels that pass from the pia mater into 
the brain. 

The outer layers of the pia mater are the most compact, and are 
covered on their outer surface by a continuous layer of endothelial cells. 
This external layer of the pia mater is often described as a separate 
membrane called the "arachnoid," but it is really only part of the pia. 

The deeper layers of the pia contain the blood-vessels. The mem- 
branes and fibres which compose the pia mater are partly coated with 
cells which have irregular and delicate cell bodies and large, distinct 
nuclei. 

In all inflammations of the pia mater, the inflammatory products reg- 
ularly collect in the spaces within it. 

Along the borders of the longitudinal fissure, and, more rarely, on 
the under surface of the brain, are a number of small, white, firm, ir- 
regular bodies— the Pacchionian bodies. They vary in their size, their 
number, and in the extent of the surface of the hemispheres which they 
cover. They may perforate the dura mater, or, more rarely, the wall of 
the longitudinal sinus, and may produce erosions of the skull bones. 
They are composed of fibrous tissue and may undergo fatty or calcareous 
degeneration. As they are so commonly found and are not known to be 
of any pathological significance, they may almost be regarded as normal 
structures; at any rate, we do not know what causes them or their varia- 
tions in size and number. 

The pia mater is frequently thickened, opaque, and white, either in 
diffuse patches or, more commonly, along the course of the vessels. In 
other cases, single or multiple small white spots, of the size of a pin's 
head or smaller, may be seen in the membrane, not appreciably elevated 
above the surface, but due to localized thickening. These slight opaci- 
ties of the pia mater are commonly believed to be dependent upon re- 
peated congestions of the membrane or upon chronic meningitis, but 
there is no evidence that this is always the case. They are most fre- 
quently found in old persons, but may exist at any age, and do not neces- 
sarily indicate the pre-existence of disease, although similar appearances 
are common in the chronic insane and in drunkards. 

The amount of blood contained in the vessels of the pia mater after 
death varies greatly, and is hj no means a reliable indication of the 
amount present during life. In general anaemia, the vessels of the pia 
mater may contain little blood, but, on the other hand, they sometimes 
seem to contain a relatively larger amount than other parts of the body. 



THE NERVOUS SYSTEM. 169 

In oedema of the brain and pia mater, the vessels of the latter may con- 
tain but a small amount of blood. 

The pia mater may be hyper cemic in early stages of meningitis, after 
death from delirium tremens, or following epileptic convulsions, from 
various infectious diseases, certain poisons, the presence of tumors or 
exudations pressing on the veins, as well as from general and local dis- 
eases of the circulatory apparatus. But whether they are overfilled or 
comparatively empty after death seems to depend upon the position in 
which the body has lain, upon the time which has elapsed between 
death and the examination, upon the rapidity with which the blood co- 
agulates, and upon conditions entirely unknown to us. 

(Edema. — The amount of serum beneath the pia mater and infiltrat- 
ing its tissue is very variable in amount. It may accumulate as a result 
of atrophy of the brain substance or of venous byperaemia, and sometimes 
is, and sometimes is not, accompanied by oedema of the brain substance. 
It may be diffuse or localized. It is not infrequent to find in hospital 
patients suffering from chronic nephritis, cardiac or pulmonary disease, 
or chronic alcoholism, a very considerable amount of serum in this situ- 
ation, and yet the patient has been free from cerebral symptoms. In 
other cases, again, this same serous effusion affords the only explanation 
of grave cerebral symptoms. It is necessary to be very careful in judg- 
ing of the importance of this accumulation of fluid. 

It should always be borne in mind that an accumulation of fluid be- 
neath and in the meshes of the pia mater may occur as a result of post- 
mortem changes. 

Hemorrhage. — This may occur either into the space between the dura 
mater and pia mater — inter meningeal hemorrhage — or in the meshes of 
the pia or between the latter and the brain. It may be due to injury, to 
rupture of aneurisms or otherwise diseased blood-vessels, to thromboses 
of the venous sinuses, or to causes which we are unable to ascertain. 
Hemorrhages, without known cause, not infrequently occur in the sub- 
stance of the pia mater in young children, but in adults they are apt to 
be the result of injury. Multiple ecchymoses, however, in the substance 
of the pia mater sometimes occur in infectious diseases and also in acute 
inflammation of the pia mater. Haemorrhages in the brain substance 
may lead to the accumulation of blood beneath or in the meshes of the 
pia mater. Intermeningeal haemorrhage in infants as a result of injury 
during birth is not uncommon. Small, and sometimes considerable, ex- 
travasations of blood may occur from diapedesis, and sometimes, as a re- 
sult of chronic congestion, degenerated blood pigment collects along the 
walls of the vessels. The extravasated blood in meningeal haemorrhage, 
if small in quantity, may be largely absorbed, leaving a greater or 
smaller accumulation of pigment at the seat of the haemorrhage, and 
such pigmentations may last for a long time. 
13 



170 



THE NERVOUS SYSTEM. 



Inflammation of the pia mater is called lepto-meningitis, or simply 
meningitis. We distinguish acute, chronic, tubercular, and syphilitic 
meningitis. 

Acute Meningitis occurs most frequently as the characteristic lesion 
of epidemic cerebro-spinal meningitis ; it is a not very infrequent com- 
plication of pneumonia, Bright's disease, typhus and typhoid fever, and 
the exanthemata; it is secondary to injuries and inflammation of the 
cranial bones, of the dura mater, and of the middle ear, and it is some- 
times an idiopathic lesion. 










Fig. 8.J.— Cellular Meningitis, x 850 and reduced. 



In any case of acute meningitis, the inflammation is apt to extend 
downward and involve the pia mater of the cord. It may also involve 
the ependyma of the ventricles, and cause the distention of these cavi- 
ties with serum. This latter condition belongs especially to young chil- 
dren. 

There are two anatomical varieties of acute meningitis, which give, 
however, the same clinical symptoms. 

(1) Acute cellular meningitis. — The pia mater is somewhat con- 
gested, its surface is dry and lustreless, and it is somewhat opaque. 
These changes in the gross appearance of the membrane are not marked, 
and are easily overlooked, but the minute changes are more decided. 



THE NERVOUS SYSTEM. 17 L 

There is an abundant production of cells somewhat resembling the cells 
which coat the surfaces of the membranes and fibres which make up the 
pia mater (Fig. 84). This cell growth is general, involving the pia 
mater over most of the surface of the brain. The inflammation, then, 
is one which results in the production, not of fibrin, serum, or pus, but 
of new connective-tissue cells. This form of meningitis is of frequent 
occurrence, and is attended with the ordinary clinical symptoms of acute 
meningitis. 

(2) Simple acute meningitis of the exudative form is characterized 
by the accumulation, chiefly in the meshes of the pia mater and along 
the walls of the blood-vessels, of variable quantities of serum, fibrin, and 
pus. Sometimes one, sometimes another of these exudations prepon- 
derates, giving rise to serous, fibrinous, or purulent forms of the inflam- 
mation. The absolute quantities, too, of the exudations vary greatly. 



% 



Fig. 85.— Acute Purulent Meningitis. 
a, convolutions of cerebrum ; 6, pia mater thickly infiltrated with pus ; c, blood-vessels entering 
brain from pia and surrounded by a zone of pus cells ; d, congested blood-vessels of pia mater ; e, 
smaller blood-vessels of pia, arouni which pus cells are collected in dense masses. 

In some cases, death may be caused with so slight a formation of exuda- 
tion that, to the naked eye, the pia mater may look quite normal or 
perhaps only moderately hyperaemic or (Edematous; the microscope, 
however, in these cases, will reveal pus cells in small numbers, and 
sometimes flakes of fibrin in the meshes and along the walls of the ves- 
sels. In other cases, turbid serum in the meshes of the membrane is all 
that can be seen, and the microscope shows the turbidity to be due to 
pus cells or a small amount of fibrin. Again, either with or without 
marked oedema of the pia mater, yellowish stripes are seen along the 
sides of the veins, sometimes appearing like faint turbid streaks, and at 
others dense, opaque, thick, and wide, and almost concealing the ves- 
sels. These are due to the accumulation of pus cells and fibrin in large 



172 



THE NERVOUS SYSTEM. 



quantities along the vessel, and they are best seen and most abundant 
around the larger veins which run along over the sulci. In still other 
cases, the infiltration with pus and fibrin is so dense, and thick, and 
general that the brain tissue, convolutions, and most of the vessels of 
the pia mater themselves are concealed by it. This is usually of a 
greenish-yellow color, and is sometimes so thick as to form a sort of cast 
of the brain surface at the seat of the lesion (Fig. 85). Sometimes ex- 
travasated red blood-cells are mingled with the other exudations as the 
result of diapedesis. Microscopical examination shows numerous white 
blood-cells sticking in the walls of the veins and capillaries, or the ves- 
sels may be blocked with them. It is evident that a large part of the 
pus cells accumulate as the result of emigration. The connective-tissue 




Pig. 86.— Fatty Degeneration op Cells along Blood-vessels op Pia Mater after Exu- 
dative Meningitis. 
From a child five years old. 



cells of the pia mater may be detached from their places or degenerated. 
In some cases, there are considerable accumulations of pus between the 
pia mater and the brain substance and along tbe vessels which enter the 
latter. More rarely pus is found upon the free surface of the mem- 
brane. The brain substance may be compressed by the accumulated 
exudation, so that the convolutions are flattened. The cortical portion 
of the brain may be simply infiltrated with serum — cedematous — or it 
may undergo degenerative changes, or it may be the seat of punctate 
haemorrhages. Not infrequently the inflammation extends to the ven- 
tricles, which may contain purulent serum, and to the pia mater of the 



THE NERVOUS SYSTEM. 173 

cord. This form of inflammation is most frequent on the convexity of 
the brain, but may extend, or even be confined to the base. It may be 
localized, but frequently extends widely over the surfaces of the hemi- 
spheres. Bacteria are often present in the exudation. For their rela- 
tionship to the lesions, see Oerebro-spinal Meningitis. 

When recovery from acute exudative meningitis occurs, there may be 
fatty degeneration of the cells which have accumulated in the pia mater, 
particularly along the vessels (Fig. 86), and this may produce white 
patches in the membrane and threads along the blood-vessels, which re- 
semble the appearance of an accumulation of exudation in the acute 
stage. Fatty degeneration of the blood-vessels and cells of the pia mater 
may also occur without acute inflammatory changes. 

Sometimes, in children and young adults, the inflammatory changes 
in the ventricles persist for days and weeks after the subsidence of the 
inflammation of the pia mater. 

Chronic Meningitis. — Either the pia mater at the base of the brain 
alone may be inflamed (basilar meningitis), or the pia mater over the 
convexity alone, or the entire pia mater, or circumscribed patches of the 
membrane. The pia mater is thickened and opaque, the thickening 
being sometimes very considerable. There is a formation of new con- 
nective tissue and a production of pus, fibrin, and serum; the relative 
quantity of these inflammatory products varies in different cases. Firm 
.and sometimes extensive adhesions may be formed between the dura 
mater and the pia mater. JSTot infrequently the cortical portions of the 
brain participate in the morbid process, and we find infiltration of small 
spheroidal cells around the blood-vessels, thickening of the walls of the 
vessels, and degenerative changes and atrophy of the nerve tissue. New 
connective tissue may also form in the brain substance, which may be- 
come closely adherent to the pia mater. The ventricles of the brain also 
may contain an increased amount of serum, and may be dilated, and the 
ependyma may be thickened and roughened. This form of inflammation 
may be the result of injury or disease of the cranial bones, or secondary 
to chronic pachymeningitis or to inflammation of the brain substance. 
It may occur in the vicinity of tumors of the brain or meninges. It 
may be a complication of chronic diffuse nephritis or the result of 
chronic alcoholic poisoning. It may occur in marked form in the 
general paralysis of the insane. 

Tubercular Meningitis. — This is especially characterized by the for- 
mation in the pia mater of miliary tubercles, associated with more or 
less well-marked exudative inflammation. It may occur in adults and 
in children, but is more common in the latter. The dura mater may be 
unchanged, or its inner surface may be sprinkled with miliary tubercles. 
The pia mater may or may not be congested; it may look dry on the 
surface or it may be oedematous. Usually the brain seems to fill the 



174 



THE NERVOUS SYSTEM. 



cerebral cavity to an unusual degree, and the convolutions are flattened. 
If the pia mater be oedematous, the serum may be clear or turbid with 
pus and fibrin. The membrane may present any of the general ap- 
pearances of exudative meningitis. But always in addition to these, and 
sometimes without them, miliary tubercles, either widely scattered or in 
great numbers, may be seen, usually more abundant over the sulci than 
elsewhere. They are usually more abundant at the base of the brain 
than on the convexity, and are frequently confined to the base. Some 
of the tubercles are so small as to be scarcely visible or entirely invisible 
to the naked eye; others are as large as a pin's head or larger. They 
are usually most abundant along the blood-vessels, but may occur else- 




Fig. 87.— A Miliary Tubercle of the Pia Mater, X 850 and reduced. 
Composed of a simple aggregation of cells. 

where. They may be formed in the membranous prolongations of the 
pia mater which dip into the sulci, around the vessels which enter the 
brain substance, in the choroid plexus and ependyma of the ventricles, 
and may exist in the spinal cord. 

The miliary tubercles do not all have the same structure. Some of 
them are simply small aggregations of round cells within the perivascular 
sheaths of the smaller arteries. Others are composed of small masses of 
polyhedral and round cells without any basement substance between 
them, and without any special relation to the blood-vessels (Fig. 87). 



THE NERVOUS SYSTEM. 



175 



Many others have the ordinary structure of tubercle tissue, basement 
substance, polyhedral cells, and giant cells. These tubercles are usually 
situated around or near a blood-vessel, and this blood-vessel is apt to 



m. 



■^gmz0^l 



Fig. 88.— A Miliary Tubercle op the Pia Mater. 
Situated on the wall of a small artery which is the seat of endarteritis. 

be at the same time the seat of an obliterating endarteritis (Fig. 81 
This form of tubercle is also prone to cheesy degeneration (Fig. 89). 




vi^-^yK-i^S 



Fig. 89.— Miliary Tubercle op the Pia Mater of a Child, undergoing Cheesy Degeneration 

at its Centre. 



In children, the ventricles are usually more or less distended by an 




2 \ * ?= 



Fig. 90.— Miliary Tubercles of the Ependyma of the Lateral Ventricle, X 70 and reduced. 

accumulation of transparent or turbid serum, and the walls of the ven- 
tricles may be studded with miliary tubercles (see Figs. 90 and 91). In 



176 



THE NERVOUS SYSTEM. 



adults, the ventricles are less frequently involved. The brain tissue 
around the ventricles is often softened. The central canal of the spinal 
cord may also be dilated. It is the dilatation of the ventricles which 
causes the flattening of the convolutions, and the flattening is usually in 
direct proportion to the amount of accumulated fluid. Miliary tuber- 
cles in the choroid of the eye are present in a considerable proportion of 
cases. 







■ i>~ 



^#-\^ 






: 










&'%'^ 



^•'-f. 




Fig. 91. — Miliary Tubercle of the Ependyma of the Lateral Ventricle, x 500 and reduced. 

The cortex of the brain may be hypersemic, and punctate haemor- 
rhages may be present in the cortex and in the pia mater. 

In almost all cases of tubercular meningitis, there is tubercular in- 
flammation in other parts of the body. 

In adults, as in children, while the tubercular inflammation is always 
present, the accompanying simple inflammation may be very slight or 
extensive, and the degree to which it develops does not seem to depend 
upon the abundance of the miliary tubercles. Owing to the frequency 



THE NERVOUS SYSTEM. 177 

of the dilatation of the ventricles with serum in children, the disease is 
often called acute hydrocephalus. 

In both children and adults, the tubercular inflammation may pro- 
duce large masses of tubercular tissue, which undergo cheesy degenera- 
tion, in the pia mater and the brain tissue. 

Syphilitic Meningitis. — In this form of inflammation, which is usually 
circumscribed, there is a development of gummy tumors of variable size, 
frequently associated with simple inflammation of the membrane, either 
with the formation of serum, fibrin, and pus, or with the development of 
new connective tissue and the consequent thickening of the membrane. 
The gummata may form in the pia mater covering the convexity, or at 
the base of the brain. They may grow outward, involving the dura 
mater; or inward, incroaching upon or involving the brain tissue. Al- 
though usually circumscribed, the syphilitic inflammation may occur as 
a diffuse thickening of the membrane. The syphilitic nodules, includ- 
ing the gummata and new-formed connective tissue, are often very small, 
but may be as large as a hen's egg. 

Tumors. — Aside from the Pacchionian bodies, which are sometimes 
so large as to simulate tumors, the most common forms of primary tu- 
mors are sarcomata and endotheliomata (cholesteatomata). Small fibro- 
mata, lipomata, angiomata, and myxomata occur, but are rare. Lym- 
phangiomatous cysts sometimes occur in the pia mater, and various forms 
of carcinoma may occur as secondary tumors. The pia mater is fre- 
quently involved in tumors growing from the dura mater or the brain 
substance. 

Variously shaped pigment cells not infrequently occur in the pia mater, 
either scattered or sometimes in considerable masses; they seem to have 
little pathological significance. Not infrequently thin plates of new- 
formed bone are found in the pia mater, associated with a thickening of 
the membrane. 

Parasites. — Cysticercus has been observed in the pia mater. 



THE VENTRICLES OF THE BRAIN. 
THE EPENDYMA AND CHOROID PLEXUS. 

As the lymph spaces of the pia mater and the ventricles of the brain 
are in communication, it might be supposed that they would share alike 
in the accumulation of fluids. This, however, is not the case. The 
membranes of the brain may be highly cedematous while the ventricles 
contain about the normal quantity of fluid; or, on the other hand, the 
ventricles may be widely dilated' and the pia mater unusually dry. Many 
of these varying conditions may be understood by remembering that the 
skull and spinal canal form a closed cavity, and that accumulations of 



178 THE NERVOUS SYSTEM. 

fluid in one part must be at the expense of some material occupying 
other parts, either blood, serum, or brain tissue. It is not always easy 
to see, however, exactly how the compensation occurs. 

There may be an unusual amount of fluid in the ventricles of the 
brain as a result of post-mortem change; in connection with senile or 
other atrophy of the brain; or in the general vascular changes which 
lead to oedema of the brainy in connection with inflammation of the 
meninges or of the ependyma; or under conditions which we do not 
understand, as in some cases of congenital and acquired hydrocephalus. 
Accumulations of fluid in the ventricles are often called internal hydro- 
cephalus, to distinguish them from accumulations in the meninges — 
external hydrocephalus. 

Acute Inflammation of the Ependyma {Acute Ependymitis). — In 
this condition, which may occur by itself, but is usually associated with 
inflammation of other parts of the brain, the ependyma is congested, 
the vessels are more prominent than usual and are often tortuous. The 
ependyma and the adjacent brain tissue may be thickened and infiltrated 
with pus cells, and the surface of the ependyma covered with fibrin and 
pus in variable quantity. The cavities of the ventricles may contain 
purulent serum. Small haemorrhages may also be present in the tissue 
of the ependyma. This, as well as other forms of inflammation, is more 
common in the lateral ventricles than in the others, but not infrequently 
involves the fourth ventricle. The choroid plexus may participate in 
the inflammatory changes of the ependyma. Tubercular inflammation 
of the ependyma is, as above mentioned, a not infrequent accompani- 
ment of tubercular meningitis. 

Chronic Inflammation of the Ependyma {Chronic Ependymitis). — 
This lesion, which is much more common than simple acute inflam- 
mation of the ependyma, occurs under a variety of conditions, and its 
nature and causation are in general very obscure. The ependyma is 
thicker, whiter, and more opaque than normal, so that the vessels may 
be nearly or quite invisible. The thickening may occur in patches or 
diffusely, and the surface of the ependyma may be smooth, or roughened 
and granular. On microscopical examination, the surface of the epen- 
dyma may be covered with the usual epithelium, but the new connective 
tissue which forms beneath it often raises it up in places, causing the 
roughness of the surface. The new tissue is usually rather loose in tex- 
ture and may contain many small spheroidal cells; but it may be dense 
in texture and contain few cells. The brain tissue beneath the thickened 
ependyma may be softened or infiltrated with cells. The sides of the 
ventricles may be grown together in places by the adhesion of the 
thickened and roughened ependyma. The ventricles usually contain 
more serum than normal, and sometimes this accumulation is so great 
as to cause an enormous dilatation of them. While these are in general 



THE NERVOUS SYSTEM. 



179 



the prominent lesions in chronic inflammation of the ependyma, the 
cases vary greatly in the degree to which these changes are developed. 

The accumulation of fluid and the dilatation of the ventricles being 
the most marked feature in all this class of lesions, they are often called 
chronic hydrocephalus, and indeed in many cases we have no evidence 
that the change in the ependyma is an important or even an actual 
primary factor. 

We may, for convenience of study, consider three classes of cases of 
chronic hydrocephalus: first, congenital hydrocephalus in young chil- 
dren; second, secondary hydrocephalus in children and adults; third, 
primary hydrocephalus in adults. 

1. Congenital Hydrocephalus. — The lesion may be in an advanced 
stage at the time of birth, or it may be scarcely evident or but mode- 
rately developed. It may progress rapidly and cause the early death of 






a —4 




Fig. 92.— Congenital Hydrocephalus in Child. About half natural size. 
a, a, dilated lateral ventricles; 6, cornua, unequally dilated; c, third ventricle; d, middle com 



the child, or it may develop gradually or come to a stand-still. In the 
more marked forms of the disease, the ventricles are widely dilated and 
filled with serum, which is usually transparent. JSTot only the lateral 
ventricles, but also the third and fifth, may be involved; the fourth is 
less apt to participate in the lesion, although it is sometimes dilated, as 
well as the central canal of the cord. 

The distention, especially of the lateral ventricles, may be so great 
that the brain tissue over the vertex is crowded up into a thin layer 
beneath the dura mater, or it may be entirely destroyed. When the 
dilatation of the ventricles is considerable, the convolutions are flattened 
(see Fig. 92) and may be almost entirely obliterated. The skull bones 
may be thin and bulging over the forehead and vertex; the fontanelles 
and sutures widely open. The ependyma in these cases is usually thick 



180 THE NERVOUS SYSTEM. 

and rough, but it may be softened, and the blood-vessels may be dilated. 
The basal portions of the brain may be flattened, but are usually muck 
less affected than the upper portions. The brain tissue is usually soft 
and anaemic. 

2. Secondary Hydrocephalus. — This may occur in children and 
adults, and may be a result of epidemic cerebro-spinal meningitis, or 
of acute meningitis, or of chronic meningitis. It sometimes occurs in 
chronic alcoholic poisoning and in general paralysis of the insane. The 
amount of dilatation of the ventricles varies greatly in these cases, but 
it is never so great as in congenital hydrocephalus, and is not accompa- 
nied by the changes in the shape of the skull which form so prominent 
a feature in the latter disease, since the bones are firmer and the sutures 
united. In this form of chronic hydrocephalus, the changes in the 
ependyma above described are usually more or less well marked, and 
they may be associated with the production of fibrin and pus. 

3. Primary Hydrocephalus in Adults. — The conditions leading to 
this form of lesion are not understood. It is apt to occur in persons 
over thirty years of age. Sometimes one, sometimes both lateral ven- 
tricles are dilated. The dilatation is usually moderate, sometimes very 
slight, and never as great as in congenital hydrocephalus. The ventri- 
cles usually contain transparent serum, and the ependyma is thickened 
and roughened. In some cases, it will be the only lesion found to ac- 
count for the death of the patient. 

Tumors. — The new formation of connective tissue in the ependyma, 
although usually diffuse, may be circumscribed and form small, project- 
ing connective-tissue nodules, which may be reckoned among t\\z fibro- 
mata. Small fibromata are sometimes detached from the walls of the 
ventricles and lie free in the cavity. Small lipomata, angiomata, and 
also sarcomata and gliomata occur rarely. Chondromata and angio- 
mata may occur in the choroid plexus, and the latter are sometimes as 
large as a hen's egg. The choroid plexus is not infrequently the seat of 
transparent cysts, usually of small size; they may contain a clear fluid 
*or colloid material, or droplets of fat or calcareous particles. A small 
dermoid cyst containing hairs has been described. These cysts have no 
special pathological significance. 

Primary carcinomata are sometimes found in the ventricles. 

The calcareous bodies called brain sand 1 occur frequently in the 
choroid plexus (see Fig. 83), and corpora amylacea may occur here and 
beneath the ependyma. 

Oysticercus and ecchinococcus cysts are sometimes found free in the 
fluid of the ventricles. 

1 The little, hard masses called brain sand consist of aggregations of small particles 
of carbonate and phosphate of lime, with a very small amount of phosphate of ammo- 
nia and magnesia. With these there is more or less organic matter. 



THE NERVOUS SYSTEM. 181 

PINEAL GLAND AND PITUITARY BODY. 

Pineal Gland. — The lesions of this structure are not very common or 
important. It may participate in inflammatory changes involving neigh- 
boring structures. It may become hypertrophied and dense, and has thus 
attained the size of a walnut. Small cysts may form in it, and of very 
frequent occurrence is a considerable increase in the amount of brain 
sand, which is usually found there in moderate quantity under normal 
conditions. 

The Pituitary Body. — This body may share in inflammatory changes 
occurring in its vicinity, or may be the seat of tubercular and syphilitic 
inflammation. The most important of the tumors which may originate 
in this structure are adenomata, usually cystic in character; these may 
be as large as a hen's egg. Carcinomata and sarcomata may occur, form- 
ing tumors of considerable size. Small livomata and a teratoma have 
been described. 

THE BRAIN. 
THROMBOSIS AND EMBOLISM. 

In studying the occurrence and effects of thrombosis and embolism 
in the brain, certain peculiarities of the circulation should be borne in 
mind. The arteries of the brain are in part terminal arteries (see page 
57), in part such as have anastomoses among their branches. Thus the 
arteries which are distributed to the cortical regions form abundant 
anastomoses in the pia mater and are very small when they enter the 
brain, while those which are distributed to the basal region, and which 
supply the basal ganglia, are larger and do not, beyond the circle of 
Willis, form anastomoses with one another. Thus it is that occlusions 
of the arteries supplying the basal ganglia are of much more serious im- 
port, aside from the importance of the parts involved, than those passing 
to the cortex. 

Thrombi may form in the arteries as a result of any degenerative or 
inflammatory process in the wall of the vessel leading to a roughening or 
death of its intima, or from pressure upon the vessel from without, or 
they may occur in vessels in whose walls we can detect no primary lesion. 
The most common causes are atheroma or simple endarteritis. Thrombi 
may also form around an embolus which does not entirely occlude the 
vessel. 

Emboli of the cerebral arteries most commonly arise from acute or 
chronic endocarditis or cardiac thrombi; they may arise from aneurisms 
or atheroma of the aorta, from the carotid or vertebral arteries, or from 
the pulmonary veins. The materials constituting emboli vary greatly, 
depending on their mode of origin (see page 56). The effects on the 



182 



THE NERVOUS SYSTEM. 



brain tissue of emboli and thrombi of the arteries are essentially the same 
in their main features. In some cases, however, in which large emboli, 
usually from endocarditis, suddenly block up a large vessel, the indivi- 
dual may die almost instantly without other apparent lesion than the 
stoppage of the vessel. 

In general, the first effect of the occlusion of an artery is to deprive 
the region to which it is distributed of blood. In arteries whose branches 
anastomose, as in the cortex of the brain, the affected area is soon sup- 
plied with blood, by the establishment of a collateral circulation. In ter- 
minal arteries, on the other hand, the blocking of the vessel is followed, 
as a rule, by degenerative changes and softening in the brain tissue. The 




Fig. 93.— Degenerated Culls, Cholestearin Crystals, and Corpora Amylacea from Brain 
Tissue in Embolic Softening. 
a, fatty ganglion cells; b, corpora amylacea; c, cell containing very large number of fat-drop- 
lets (compound granular or Gluge's corpuscles) ; d, cholestearin crystals. 



appearances which these degenerated areas present vary greatly, depend- 
ing upon the stage of the degeneration and the amount of blood which 
may be extravasated. Dense infiltrations of the brain tissue with blood, 
as in hemorrhagic infarctions from emboli in other parts of the body, 
do not usually occur, although considerable blood may be extravasated. 
Areas of softening in which there is little extravasation of blood are usu- 
ally white or yellow in color {white or yellow softening). When much 
blood is present, the process is frequently called red softening. The 
tissue in the affected area gradually softens and may become diffluent*. 



THE NERVOUS SYSTEM. 



183 



Microscopically, the softened tissue is seen to consist of more or less fluid 
with broken-down brain tissue, fragments of nerve fibres, droplets of 
myelin, nerve cells, shreds of neuroglia tissue and blood-vessels, and red 
and white. blood-cells. Then evidences of degeneration are seen in the 
presence of fat grannies and droplets, larger and smaller cells densely 
crowded with droplets of fat (so-called Gluge's corpuscles or compound 
granular corpuscles) (see Fig. 93). Various kinds of cells and cell 
fragments, more or less granular and fatty, and also corpora amylacea, 
blood-pigment, fat- crystals, and cholestearin crystals, may be found. The 
walls of the blood-vessels may also be in a condition of fatty degeneration 
(Fig. 94). The color of the softened mass will of course depend upon 
the relative amounts of these elements. 

The tissue may remain for a long time in the soft condition, or it 
may be absorbed and replaced by a connective-tissue cicatrix, which may 




Fig. 94.— Blood-vessels from an Area of Embolic Softening of Brain. 
The walls of the vessels, particularly the endothelial cells, contain fat-granules and fat-droplets. 



be more or less pigmented; or a wall of connective tissue may form about 
it, converting it into a well-defined cyst, with or without pigmented 
w r alls; or the mass may dry and form a dense, structureless nodule. 
Acute inflammatory changes may occur about the dead tissue. In cases 
of infectious emboli, numerous abscesses may be formed in addition to 
their mechanical action. 

Thrombi are most frequent in the internal carotids, less so in the 
middle cerebral, basilar, and vertebrals. They may occur, but still less 
frequently, in other cerebral arteries. Emboli are most common in the 
middle cerebral artery, next in the internal carotid, and then in the 
basilar. The relative frequency with which embolism occurs in the 
middle cerebral artery is attributable to the directness with which the 
blood passes into this artery from the heart. The great significance 
attaching to embolism of the middle cerebral artery is evident when we 



184 THE NERVOUS SYSTEM. 

remember that its branches are terminal arteries, and are distributed to 
such important structures as the lenticular and caudate nucleus, the in- 
ternal capsule, and the optic thalamus. 

Hypercemia and Anaimia. — The appearance of the brain tissue after 
death does not always furnish reliable indications of its blood-contents 
during life, though they are perhaps more to be depended on than the 
appearance of the meninges. 

Some of the more common conditions determining hyper cemia which 
are mentioned above as influencing the meninges, apply also to the 
substance of the brain. In sections of hyperaemic brains, the small 
blood-points from the cut ends of small vessels are more numerous and 
conspicuous than under normal conditions, and the brain tissue, particu- 
larly the gray matter, may have a diffuse red color. If excessive, the 
convolutions may be somewhat flattened, and the brain tissue and pia 
mater may be cedematous, and the ventricles contain fluid. The con- 
gestion of the vessels may be general or localized. 

Anmmia of the brain may be either local or general. It may depend 
upon a general anaemia or upon general disturbances of the circulation, 
such as mitral stenosis or regurgitation, or upon local interference with 
the arterial blood-supply, such as complete or partial obstruction of the 
arteries from thrombi, emboli, inflammatory changes, spasmodic con- 
tractions, etc., or from tumors, exudations, and blood-extravasations 
pressing upon the vessels from without. In oedema of the meninges, 
and in the presence of internal hydrocephalus, the brain tissue is apt to 
be anaemic. The brain tissue in anaemia looks whiter than usual, the 
contrast between the gray and white matter is less marked, and the 
small blood-points usually seen on section from divided vessels may be 
very inconspicuous or almost entirely absent. 

(Edema of the brain tissue may accompany either hyperaemia or 
anaemia, and seems in most cases, though not always, to be dependent 
upon conditions which induce these alterations in the blood-contents of 
the brain. In some cases of marked impoverishment of the blood, a so- 
called hydramiic oedema of the brain is found. Very marked oedema of 
the brain may exist without any accompanying brain symptoms. On 
the other hand, persons may die comatose; this is seen with especial fre- 
quency in acute and chronic alcohol poisoning, but may occur under 
other conditions, and the post-mortem examination reveals nothing but 
oedema of the brain tissue, either with or without oedema of the pia 
mater. 

Hemorrhage. — Haemorrhages in the substance of the brain may be 
very small and punctate, and are then usually called capillary haemor- 
rhages, or they may result in the collection in the brain tissue of masses 
of blood of considerable size, which are called apoplectic foci or clots. 



THE NERVOUS SYSTEM. 185 

These forms of haemorrhage may be associated, or a number of capillary 
haemorrhages may join to form an extensive clot. 

Capillary haemorrhages may look, on section of the brain, like the 
severed ends of hyperaemic blood-vessels, or the tissue about them may 
be more or less tinged with blood. Microscopically, the perivascular 
spaces will be found distended with blood, which may have escaped into 
them and more or less broken down the brain tissue. They may occur 
singly, but are frequently multiple, so that the brain tissue is besprinkled 
with blood-points. Degeneration of the extravasated blood may give 
rise in later stages to reddish or brown or yellowish circumscribed dis- 
coloration of the brain tissue, due to granules and crystals of blood- 
pigment intermingled with broken-down brain tissue, with more or less 
fatty degeneration of its elements. Capillary haemorrhages may be due 
to fatty degeneration of the vessels leading to rupture; or the extrava- 
sation may be due to diapedesis, or it may depend upon conditions 
which we do not understand. They frequently occur in the vicinity of 
apoplectic clots and tumors; they may be due to thrombosis of the veins, 
or of the sinuses of the dura mater; they not infrequently occur in acute 
encephalitis, in congestive hyperaemia, in acute mania, and in delirium 
tremens; and they may be associated with general diseases, such as 
scurvy, purpura baemorrhagica, typhus fever, pyaemia, ulcerative endo- 
carditis, etc. ; they may be associated with embolic softening. 

Apoplectic foci may result from the coalescence of numerous capillary 
haemorrhages: from injury, or from rupture of diseased arteries, either 
with or without changes in the blood-pressure. Haemorrhages from in- 
jury to the skull may occur as well without as with fracture, and may 
be situated over the vertex as well as at the base of the brain, and 
vary in extent and seat, depending upon the character and point of the 
injury and the size of the vessels involved. The so-called spontaneous 
haemorrhages, other than those of capillary origin, which give rise to 
masses of blood and broken-down brain tissue, may vary in size from 
that of a pea to those occupying a large part of a hemisphere. They are 
due in a very considerable proportion of cases to the rupture of small 
arterial aneurisms, but may arise from weakening of the walls of the 
arteries, from arteritis, atheroma, or fatty degeneration. These latter 
forms of disease doubtless give rise in most cases to the formation of the 
aneurisms whose rupture is in so many cases the immediate cause of the 
haemorrhage. Aneurisms of the cerebral arteries may be as large as a 
pea or hazelnut, but those most frequently met with and causing apo- 
plexy are usually small — called miliary aneurisms — and may be micro- 
scopic in size, varying from this up to that of a large pin's head or larger. 
They may be sacculate or fusiform, and frequently exist in considerable 
numbers. They may occur in any of the small arteries of the brain, but 
are said to be most frequent on the branches of the middle cerebral 
14 



186 THE NERVOUS SYSTEM. 

artery. It is asserted that the bursting of miliary aneurisms is the nearly 
if not quite exclusive cause of the formation of spontaneous apoplectic 
clots, but this we do not believe to be true. As to the immediate cause 
of rupture, either of aneurisms or otherwise diseased blood-vessels in the 
brain, we are in many cases entirely ignorant. In some cases it seems 
to be due to an increased arterial tension in such diseases of the heart as 
induce this change, as in the cardiac hypertrophy which may accompany 
some forms of chronic diffuse nephritis; or it may result from unusual 
exertion or mental excitement; but, as above stated, in many cases the 
immediate inciting cause is not evident. 

The most frequent seat of hemorrhage is in the corpora striata and 
optic thalami and the brain tissue in their vicinity, and here they occur 
most often in the parts supplied by the branches of the middle cerebral 
artery. The possibility of hemorrhage in the floor of the fourth ven- 
tricle as a cause of sudden death should be borne in mind in investi- 
gating cases of sudden death from obscure causes. 

Hemorrhages frequently seriously affect other portions of the brain 
than those immediately supplied by the ruptured vessels. Thus hemor- 
rhages in the cortical substance or beneath the pia mater may force their 
way deep into the brain substance; or, in hemorrhage in the brain sub- 
stance, the blood may burst into the ventricles or work its way into the 
intermeningeal space, and either at the seat of its occurrence, or in the 
situations into which it is forced, it may give rise to serious compression 
of the brain. Portions of the brain containing large extravasations may 
be enlarged, the tissue anemic from pressure, the convolutions flattened, 
and the surface dry. As the blood is poured out, the brain tissue is 
usually torn and lacerated, so that the apoplectic clot usually consists of 
detritus of brain tissue intermingled with blood. If, however, the blood 
is poured out from a single vessel, the lacerated brain tissue may be 
pressed aside, and the greater portion of the red mass may consist of 
pure blood-clot. 

The appearances presented by hemorrhages in the brain vary greatly, 
depending upon the time which has elapsed since their occurrence. If 
life continue, the oedema which usually soon occurs in the vicinity of the 
hemorrhage disappears, and the clot becomes drier and firmer; gradually 
the blood undergoes the usual series of changes seen in extravasation: 
the hemoglobin decomposes, forming granules and crystals of blood pig- 
ment; the blood-cells and fibrin undergo degeneration and absorption; 
the detritus of brain tissue undergoes fatty degeneration. As these 
alterations occur, the color changes to reddish brown, orange, or yellow, 
and the adjacent brain tissue may be discolored by imbibition. 

Inflammatory reaction may occur in the vicinity, either leading to 
the formation of a more or less pigmented cicatrix, or to a cyst with yel- 
lowish fluid contents and a fibrous, more or less pigmented wall. The 



THE NERVOUS SYSTEM. 187 

process of degeneration and absorption of the blood and broken-down 
brain tissue, and their replacement by a cyst or by a cicatrix, is a slow 
one, and the cysts and cicatrices may resemble those formed at the seat 
of embolic softening. Not infrequently we find in the brain of a person 
dead from recent apoplexy the remains of old clots presenting some one 
of the above-described stages of absorption. The apoplectic cysts and 
cicatrices persist for a long time after their formation. 

Secondary Degenerations. — Lesions of parts of the brain which in- 
volve the destruction of brain tissue containing certain systems of motor 
nerves, owing, it is believed, to the separation of these nerves from their 
trophic centres, are regularly followed after a time by degenerative 
changes in these nerves below the seat of lesion. It is particularly 
lesions in the central convolutions, the internal capsule, portions of the 
corona radiata, and the pes peduncuh, which destroy the motor fibres 
passing through these parts, and are followed by degenerative changes 
in the fibres below. The most important and frequent lesions followed 
by this effect are those involving the anterior two-thirds or three-fourths 
of the internal capsule. It will suffice merely to mention these changes 
here, as they are considered more in detail in the section devoted to 
lesions of the spinal cord. 

INFLAMMATION" OF THE BRAIN (ENCEPHALITIS). 

It has been already mentioned that the brain tissue about haemor- 
rhages and areas of embolic and thrombotic softening may undergo 
inflammatory changes leading to the formation of new connective tissue. 
There is a class of cases in which localized areas of the brain undergo 
softening, with more or less extravasation of red and white blood-cells 
and hyperemia of the blood-vessels, so that the softened material con- 
sists, as seen under the microscope, of detritus of brain tissue in a con- 
dition of fatty degeneration, with more or less pus-cells or pigment. 
When such areas are red in color from intermingled blood-cells or pig- 
ment, the condition is called red inflammatory softening. When fatty 
degeneration prevails, and the red blood-cells or their derivatives are not 
abundant, the softened area looks yellow or yellowish white, and this is 
often called yellow inflammatory softening. The origin of these pro- 
cesses is very obscure, and their inflammatory nature not well defined. 

Abscess of the Brain. — The small, multiple abscesses of the brain 
which occur with pyaemia form part of that disease and require no sep- 
arate description. 

The large, single abscesses occurring under different conditions are 
those to which the name of " abscess of the brain " is usually applied. 

These abscesses occur in two forms: 

The non-capsulated abscess, an irregular cavity containing thin pus 
and softened brain tissue. The walls of the cavity are ragged and infil- 



188 THE NEKVOUS SYSTEM. 

trated with pus, and outside of the walls is a zone of cedematous and 
softened brain tissue. If the abscess is near the pia mater, it may set up 
a meningitis; if it is near the lateral ventricles, it may rupture into 
them; if it is near the sinuses of the dura mater, it may cause throm- 
bosis. 

The incapsulated abscess has a capsule of connective tissue, and con- 
tains thin or cheesy pus. 

Abscesses of the brain are usually single; they may attain a consider- 
able size. They are most frequent in the cerebral and cerebellar hemi- 
spheres, rare in the central ganglia, the pons, and the medulla oblongata. 

The most common cause of this disease seems to be chronic sup- 
purative otitis (42.5 per cent, Gowers), while acute otitis is a compara- 
tively rare cause. With the otitis there may also be caries of the tem- 
poral bone, suppuration of the mastoid cells, and inflammation of the 
dura mater. The abscess is usually situated deep in the brain; only 
rarely is it continuous with the inflamed dura mater and bone. When 
the abscess is deeply situated, and the bone and dura mater are not dis- 
eased, it is difficult to tell how the infection travels from the ear to the 
brain. Abscesses due to this cause are situated in the temporo-sphenoi- 
dal, the frontal, the occipital, and the parietal lobes, or in the cere- 
bellum. 

Another frequent cause of abscess of the brain is traumatism — blows 
or falls on the head (twenty -four per cent, Gowers). Such injuries may 
not hurt the skull, or may produce fractures or necrosis. There is 
often a considerable interval between the time when the injury is in- 
flicted and that when the symptoms of the abscess are developed. 

When the cranial bones are uninjured, the abscess is situated deep in 
the brain; when there is necrosis of the bones, the abscess may be super- 
ficial; when the bones are fractured, the abscess may be either superficial 
or deep. The abscess is regularly situated beneath the point of injury, 
rarely in the opposite side of the brain. 

Chronic disease of the nose, either the mucous membrane or the 
bones, has been the cause of a few abscesses in the frontal lobes. Dis- 
ease of the orbit has also given rise to abscesses in the same position. 
In a few cases, the abscesses have been due to caries of various portions 
of the cranial bones. 

In a considerable number of cases (one-sixth, Gowers), no cause for 
the abscess has been discovered. 

Very frequently in acute meningitis there is an infiltration of pus 
cells along the walls of the vessels which enter the brain from the pia 
mater; and under a variety of conditions which we do not understand, 
as in some cases of typhoid fever, delirium tremens, erysipelas, and 
under many other conditions, there are numerous and sometimes very 
large numbers of leucocytes scattered through the substance of the brain, 



THE NERVOUS SYSTEM. 189 

sometimes around the ganglion cells, sometimes along the vessels in the 
perivascular sheaths. 

Chronic Interstitial Encephalitis — Sclerosis. — This lesion of the brain 
tissue may occur diffusely, occupying an entire lobe or more or less of 
the whole brain, or in circumscribed small areas. It consists essentially 
in an increase of the connective-tissue elements, the neuroglia, and an 
atrophy of the nerve elements, particularly the ganglion cells and the 
medullary sheaths of the nerves. With these changes are usually asso- 
ciated the formation of G-luge's corpuscles, corpora amylacea, granular 
and fatty degeneration of the nerve elements, and thickening and pro- 
liferation of cells of the walls of the blood-vessels. The areas of sclerosis 
may be very dense and hard, or gelatinous in consistency. 

The diffuse form of sclerosis is most frequently seen in general paresis 
of the insane, and not infrequently in the brains of drunkards. 

The circumscribed form of sclerosis, multiple sclerosis (sclerose en 
plaque), is much more common than the diffuse form, and may occur in 
the brain alone, or may be associated with a similar lesion in the spinal 
cord. It is almost entirely confined to the medullary substance, and the 
areas of sclerosis vary in size from that of a pea to that of an almond. 
They may be few or numerous, they may be white, grayish, or grayish 
red in color, and are usually, but not always, sharply outlined against 
the unaltered brain tissue. Although in many cases the increase in the 
connective-tissue elements seems to be the primary lesion, and the de- 
generation of the nerve elements secondary to this, it is quite possible 
that in some cases the increase in connective tissue may be secondary to 
a degeneration of the nerve elements from loss of nutrition or from 
other causes. 

WOUNDS OF THE BRAIN. 

The brain may be directly wounded by a foreign body, or iudirectly 
by fragments of bone driven into it, or it may be lacerated by severe con- 
tusion without fracture or solution of continuity of the skull. It is very 
difficult to estimate the degree of injury which must cause death, since 
persons frequently die from slight, and may recover from very severe,, 
wounds of the brain. In incised wounds of the brain, more or less 
haemorrhage occurs at the seat of lesion, and the brain tissue in the 
vicinity soon undergoes degenerative changes. These may be compara- 
tively slight or extensive. Inflammatory reaction may occur in the 
vicinity, and the adjacent brain tissue, as well as the hemorrhagic and 
degenerated area, become infiltrated with, pus cells. After a time the 
injured and degenerated area may become surrounded by new-formed 
connective tissue, and the decomposed extravasated blood and detritus 
of brain tissue, more or less fatty, may be absorbed, and thus after a 
time the part heals by a more or less pigmented cicatrix. The healing 
is in most cases very slow and may occupy months or even years. The 



190 THE NERVOUS SYSTEM. 

pia mater may participate to a marked degree in the inflammatory heal- 
ing process. Abscesses may form near the seat of injury. 

After wounds which involve the removal of portions of the cranial 
bones, it is not uncommon after a few days to see a bleeding fungous 
mass project through the opening. This mass, sometimes wrongly called 
hernia cerebri, consists of degenerated brain tissue, blood, and granula- 
tion tissue, with more or less pus. The brain tissue below it is degene- 
rated, broken down, soft, and purulent, and there is often abscess in the 
adjacent brain tissue. Such wounds may finally heal by the absorption 
of the broken-down brain tissue and blood, and its substitution by 
granulation tissue. 

Lacerations of the brain tissue without fracture may appear shortly 
after the injury as simple more or less circumscribed areas of capillary 
haemorrhage; the brain tissue about these may degenerate, pus may 
form, and abscesses be developed; or the degenerated and lacerated 
tissue may be gradually replaced by granulation tissue which finally 
forms a cicatrix. The process of degeneration aud softening and of 
healing in such lacerations of brain tissue may occur very slowly indeed, 
even occupying years, and not infrequently the degenerative changes 
are very extensive and progressive. In many cases, of course, the injury 
is so extensive, or involves such important parts of the organ, that very 
little or no inflammatory or degenerative change takes place before the 
occurrence of death. 

Encephalitis in the New-horn. — This condition, first described by 
Virchow, is said to consist in the formation of circumscribed collections 
of cells of various sizes containing many fat-granules (granular corpus- 
cles) and forming yellowish masses, from 1 mm. to 6 mm. in diameter, 
in the brain tissue. A more diffuse occurrence of granular corpuscles 
is also described, but this is said by some observers to be physiological. 
The nature of this lesion is but little understood, and is still the subject 
of controversy. 

Holes or Cysts in the Brain. — Larger and smaller holes may be found 
in the brain tissue from dilatation of the perivascular lymph spaces, or 
well-formed cysts may exist from haemorrhage, inflammatory softening, 
hydatids, etc. There are, however, cases in which one or several holes 
of varying size are found in the brain which cannot be determined to 
have either of the above modes of origin. They may lie deep in the 
brain substance or close under the pia mater, or may communicate 
with the ventricles. This condition is sometimes called porencephalic, 
and may co-exist with various mental aberrations, hydrocephalus, etc. 1 

Syphilitic Inflammation of the Brain sometimes results in the forma- 

1 Consult Kundrat, "Die Porencephalic," Graz, 1882, and Savage and White, 
" On the Causes of Holes in the Brain," Trans. London Path. Soc., Vol. 34, page 1, 

1888. 



THE NERVOUS SYSTEM. 



191 



tion of so-called gummy tumors. These are most frequently found near 
the periphery of the brain, not infrequently connected with the me- 
ninges, and may be sharply circumscribed. The central portion of the 
tumor is usually in a condition of cheesy degeneration, and in the peri- 
phery we see fibrous tissue or a dense infiltration of small spheroidal 
cells. 

Syphilitic inflammation of the brain very frequently occurs in a dif- 
fuse form, characterized by the formation of a gelatinous grayish tissue 











^axi&U^fa 









Fig. 



*-fl 



)5.— Syphilitic Obliterating Endarteritis of a Cerebral Artery, x 50 and reduced. 





consisting of a more or less homogeneous or granular basement sub- 
stance, with numerous small spheroidal cells. The nerve elements are 
atrophied. Obliterating endarteritis may occur as a result of syphilitic 
poisoning (Fig. 95). 

Tubercular Inflammation of the brain substance usually manifests 
itself in the formation of circumscribed masses of new tissue from 5 mm. 
to 6 mm. in diameter, or larger. These may be single or multiple, are 
most common in young persons, and very frequently occur in the cere- 
bellum. They are apt to occur in connection with tubercular inflamma- 



192 THE NERVOUS SYSTEM. 

tion of other organs. They are frequently called solitary tubercles, and 
usually consist of a dense central cheesy mass, around which is a gray- 
ish zone containing tubercle granula, numerous small spheroidal cells, 
with occasionally larger polyhedral cells and giant cells (Fig. 96). They 
do not, as a rule, seem to be formed by an aggregation of miliary tuber- 
cles, although these may be present in the periphery. Tubercle bacilli 
have been found in these solitary tubercles. 

They sometimes suppurate and break down, and then may simulate 
simple abscesses. 

Conglomerate and scattered miliary tubercles of the ordinary form 






V 


(, 






— m 







Fig. 96.— Solitary Tubercle of Cerebellum. 
a, a, miliary tubercles with giant cells ; b, b, miliary tubercles without giant cells ; c, diffuse 
tubercle tissue; d, central cheesy mass; e, nerve tissue of the cerebellum. 

sometimes occur in the brain, usually in connection with tubercular 
inflammation of the meninges or ependyma. 

LESIONS OF THE BRAIN IN GENERAL PARESIS OF THE INSANE. 

The changes in this disease are in the main those of chronic diffuse 
encephalitis, but the appearances vary greatly and depend to some 
extent upon whether the brain is examined in early or late stages of the 
disease. According to Meyer, in the early stages of the disease, the 
convolutions, particularly of the anterior cerebral lobes, are swollen, the 



THE NERVOUS SYSTEM. 193 

gray matter congested and softened in places. The brain tissue is 
more or less infiltrated with leucocytes. Fatty degeneration of the 
walls of the capillaries, and punctate haemorrhages, are also common. 

In later stages of the disease, a great variety of changes may be ob- 
served: haemorrhagic pachymeningitis, thickening of the dura mater, 
and close adhesions to the skull; thickening and opacities of the pia 
mater, adhesions of the latter to the dura mater and to the brain tissue. 
The brain tissue is apt to be atrophied, and the ventricles dilated and 
filled with fluid. The pia mater may be cedematous, the ependyma 
thickened a,nd roughened. On microscopical examination, the neuroglia 
is found to be increased in amount, the ganglion cells shrunken and 
sometimes pigmented; the nerve fibres may also be atrophied, and the 
blood-vessels in a condition of fatty or hyaline degeneration. There may 
be an accumulation of fatty and granular cells along the walls of the 
blood-vessels. Secondary degenerations in the spinal cord are not in- 
frequently observed. 

It is very difficult to make positive and definite statements regarding 
many such lesions of the brain as those just indicated, or in general of 
brain lesions whose nature must be revealed by microscopical study, be- 
cause our technical procedures in the study of the brain, even in normal 
conditions, are still quite unsatisfactory and incomplete. The brain 
tissue is so delicate and liable to post-mortem changes, and the effects 
of different, preservative agents are so liable to variations, that great 
caution is necessary in arriving at conclusions regarding the minuter 
lesions affecting the nerve tissue of the brain. 

HYPERTROPHY AND ATROPHY OF THE BRAIN. 

True Hypertrophy of the brain is rare, and probably always congen- 
ital. An increase in the size of the brain from the proliferation of the 
neuroglia sometimes occurs in children either before or after birth, less 
frequently in youth, and very seldom in adults. The white substance 
of the hemispheres is increased in amount. If it takes place before the 
ossification of the cranium, the bones are separated at the sutures and 
fontanelles; if after this, the inner table of the skull may be eroded and 
thinned. When the cranium is opened, the dura mater appears tense 
and anaemic, the convolutions of the brain are flattened, the brain sub- 
stance is firm and anaemic, the ventricles are small, the ganglia and 
cerebellum are either of normal size or compressed. 

The disease is usually very chronic, and destroys life with symptoms 
of compression of the brain. There may, however, be acute exacerba- 
tions. 

Atrophy. — This may occur as a senile change, or, in adults, in chronic 
alcohol, opium, or lead poisoning, in chronic insanity, and in chronic 



194 THE NERVOUS SYSTEM. 

meningitis. In children who are much reduced by chronic diseases, 
atrophy of the brain may accompany atrophy of the rest of the body. 

The atrophy affects principally the cerebral hemispheres, and may be 
uniform or more marked in some parts than in others. The convolu- 
tions are small,, the sulci broad, the ventricles usually dilated, the brain 
tissue firm, the gray matter discolored, the white substance grayish in 
color; the blood-vessels may be dilated. The basal ganglia may be small. 
Serum accumulates in the pia mater and the ventricles; the pia mater, 
and often the skull, become thickened; the brain tissue may be cedema- 
tous. or contain small haemorrhages. The nerve elements of the brain 
tissue are those most involved in the atrophy. 

Pigmentation. — This may occur in any portion of the brain or its 
meninges from the decomposition of extravasated blood. In persons 
affected by malaria, the gray matter of the brain has sometimes an un- 
usually dark or even blackish appearance. This color is due to the pres- 
ence of black pigment granules within the capillary blood-vessels. The 
obstruction to the vessels by masses of these pigment granules may cause 
capillary apoplexies. The pigment may also be found in the walls, and 
in the lumina of the vessels of the pia mater. 

Pigmented patches of congenital origin are not infrequently seen in 
the pia mater. They may be due to the presence of branching pig- 
mented cells. 

TUMORS OF THE BRAIN. 

The most common tumors of the brain are gliomata. They are most 
frequently found in the cerebrum, and maybe small or large. They 
may be sharply circumscribed or merge imperceptibly into the brain 
substance. They may be white and hard, or gray and soft or gelatinous. 
The softer forms consist largely of neuroglia cells (Fig. 61), the harder 
forms contain fewer cells and numerous interlacing fibrils (Fig. 60). 
The blood-vessels of the gliomata are often widely dilated. They are 
frequently the seat of haemorrhages and may soften and break down, and 
may then resemble apoplectic clots. They are liable to undergo fatty 
and cheesy degeneration. 

Not infrequently the gliomata are combined with sarcomata, forming 
glio- sarcomata. Sarcomata of various forms occur in the brain as pri- 
mary tumors. 

Circumscribed masses of dilated blood-vessels, angiomata, are not in- 
frequently met with in the brain. Myxoma, fibroma, lipoma, and 
osteoma are among the rarer forms of brain tumors. Endotlieliomata 
(cholesteatomata), in the form of glistening white tumors, sometimes 
attain a large size. Sarcomata and carcinomata not infrequently occur 
in the brain as secondary tumors. Dermoid and other cysts occur, but 
are rare. 



THE NERVOUS SYSTEM. 195 

Small masses of the gray matter of the brain sometimes occur in the 
medullary portions of the brain, and localized hyperplasias of gray matter 
have been described in the form of rounded nodules projecting from the 
free surface of the brain or into the ventricles. 

PARASITES. 

Cysticercus and, more rarely, echinococci are found in the brain. 

MALFORMATIONS. 

Cyclopia. — This malformation consists in an arrest of development 
affecting the cerebrum, which, instead of separating into two hemi- 
spheres, remains single, with one ventricle, and the rudiments of the 
eyes usually become joined and form oue eye. This single eye is in the 
middle of the face, near the place of the root of the nose, in a single 
orbit. Over this is an irregular body representing the nose. The rest 
of the face is well formed. Or the eyeball may be wanting entirely, or 
there are two eyes joined together, or, more seldom, two separate eyes. 
The orbit is surrounded by rudiments of four eyelids. The frontal bone 
is single, the nasal bones undeveloped; the ethmoid, vomer, and tur- 
binated bones are absent. The optic nerve is double, single, or absent. 
There may be hydrocephalus. Such children are incapable of prolonged 
existence. • 

Anencephalia. — This malformation may be of various degrees. The 
Drain may be entirely absent, and the base of the cranium? is covered with 
a thick membrane, into which the nerves pass. Or the membranes may 
form a sort of cyst containing blood and serum, or portions of brain. 
Of the cranial bones, only those which form the base of the skull are 
present (Acrania). The scalp is usually partly or entirely absent over 
ihe opening in the skull; the eyes stand prominently out, and the fore- 
head slopes sharply backward. This malformation may occur in other- 
wise well-developed children. 

Hydrocephalus. — This lesion has been already considered on p. 179. It 
is probable that in some cases hydrocephalus interims is due to a primary 
partial anencephalia, and that the accumulation of fluid is of secondary 
occurrence. In rare cases, only part of one lateral ventricle is hydro- 
cephalic, giving to the head a protuberance on one side. The viability 
of the foetus depends upon the degree of the hydrocephalus. Hydro- 
cephalus extemus is an accumulation of serum beneath the pia mater, 
or, according to some authors, between the pia and dura mater. It 
causes dilatation of the cranium and compression of the brain. It is 
of very rare occurrence, and may also be secondary to partial anence- 
phalia. 

Cephalocele, or Brain Hernia. — When abnormal openings exist in the 
skull from malformation, the contents of the cerebral cavity are apt to 



196 THE NERVOUS SYSTEM. 

protrude in the form of larger or smaller sacs. This may occur in cases 
of well-marked anencephalia, or in cases in which the brain is well devel- 
oped. The protruding sac formed of the meninges may or may not be 
covered with skin. If the contents of the sac are simply fluid, the lesion 
is called hy dr omening ocele; if composed of brain substance, encephalocele; 
if the sac contain both fluid and brain substance; it is called hydrence- 
phalocele. The sacs may be very small or as large as a child's head. 
They may protrude from the top of the skull in acrania. They most 
frequently protrude through openings in the occipital bone, often hang- 
ing down in large sacs upon the neck; also at the root of the nose, along 
the line of the sutures, at the base of the skull, and elsewhere. 

Microcephalia. — This is an abnormally small size of the brain, with 
a correspondingly small cranium. The diminution in size affects prin- 
cipally the cerebral hemispheres, though the other parts of the brain are 
also small. The convolutions are few and simple, the cavities often di- 
lated with serum; on the membranes there may be traces of inflamma- 
tion. The cranium is small, the face large, the rest of the body small. 
The malformation is in some cases caused by inflammation or dropsy of 
the brain during foetal life. It is endemic in some countries, but single 
cases may occur anywhere. The foetus is viable. Absence or incomplete 
development of portions of the brain may occur, not only in idiots, but 
in persons whose minds are perfect. 



THE SPIRAL COED. 



THE MEMBRANES OF THE SPINAL CORD. 
A. — THE DUKA MATER SPINALIS. 

The dura mater spinalis, unlike that of the brain, does not serve as 
periosteum to the bones forming the cavity, so that the lesions of the two 
membranes differ somewhat. Hemorrhage may occur, as the result of 
injury, between the dura mater and periosteum, or it may occur in 
tetanus, as a result of circulatory changes induced by muscular spasm, 
or in the asphyxia of new-born children. Small haemorrhages on the 
surfaces of the membrane may occur as the result of inflammation. 

Serous fluid may accumulate outside of the dura mater as a result of 
post-mortem changes, or in connection with circulatory or inflammatory 
changes in the membranes. 

Inflammation. — Acute external pachymeningitis is almost always sec- 
ondary to disease or injury of the spinal column, and may result in col- 
lections of pus between the dura mater and periosteum, usually most 
abundant posteriorly. Hemorrhagic pachymeningitis occurs in the dura 
mater spinalis, with the formation of products similar to those observed 
in the brain, in the chronic insane and in drunkards. Simple chronic 
pachymeningitis interna, with the formation of new connective tissue 
containing brain sand, is not infrequent. The new tissue may form 
minute projections or roughness of the surface, or, when more abundant, 
the psammomata. Tubercular inflammation of the dura mater spinalis 
may occur in connection with tubercular meningitis, or secondary to 
tubercular inflammation of the vertebrae. 

Tumors. — Fibromata, lipomata, chondromata, myxomata, endothe- 
liomata, and adeno- sarcomata 1 occur in the dura mater spinalis as primary 
tumors. Carcinomata and sarcomata may occur as secondary tumors. 
Small plates of new-formed bone are rarely found in the dura mater 
spinalis. 

1 Hodenpyl : American Journal of the Medical Sciences, March, 1888. 



198 THE SPINAL CORD. 

Parasites. — Echinococcns developing outside of the spinal canal may 
perforate the dura mater; or the cysts may lie between the dura mater 
and the pia mater. 

It is obvious that even small tumors in the spinal canal may give rise 
to serious results from compression. 



B. — THE PIA MATER SPINALIS. 

It is almost impossible in most cases in the pia mater, as well as in 
the dura mater spinalis and in the spinal cord, to judge with certainty, 
from the appearances after death of the blood-contents of the vessels, of 
these parts during life. The same is true of abnormal quantities of se- 
rum found after death. The veins of the pia mater, especially in the 
posterior region, may be greatly distended with blood after death, with- 
out pre-existing disease; and theintermeningeal space may contain much 
fluid under the same condition. 

Hemorrhages may occur from injury in connection with severe con- 
vulsions, or general diseases such as the hemorrhagic diathesis, scurvy, 
small-pox, etc. The haemorrhages under these conditions, except from 
injury, are not usually extensive. But in some cases of injury, or cere- 
bral apoplexy; from the bursting of aneurisms of the basilar or vertebral 
arteries; or in cases in which we cannot find a cause, a very large quantity 
of blood may collect between the dura and pia mater, and in the meshes, 
of or beneath the latter. 

Inflammation. — Acute exudative spinal meningitis occurs under 
essentially the same conditions and with essentially the same post-mor- 
tem appearances as acute cerebral meningitis, though it is less frequent- 
The exudations are apt to be most abundant in the posterior portions. 
It may be associated with a similar inflammation of the pia mater cere- 
bralis, and the inner surface of the dura mater may be involved. The 
disease may be circumscribed, but usually affects the entire length of 
the membrane. 

Tubercular inflammation is usually most marked, when associated 
with a similar condition of the pia mater cerebralis, in the upper por- 
tions of the cord; but it may extend over the entire membrane. The 
conditions under which it occurs and the character of the lesions are 
similar in both. Chronic spinal meningitis is not infrequent, mani- 
festing itself in the formation of larger or smaller patches of new con- 
nective tissue or thickenings of the pia mater. The pia and dura mater 
may thus be firmly united in places by adhesions, or the pia mater may 
become closely adherent to the substance of the cord. 

Not very infrequently large numbers of pigment cells are found in 
the pia mater spinalis, sometimes giving it a distinct gray or blackish: 
color. 



THE SPINAL CORD. 199 

Tumors. — Small plates of cartilage and bone are sometimes found in 
the pia mater. 

Fibromata, myxomata, sarcomata, and endotheliomata have been 
found. 

Parasites. — Cysticercus sometimes occurs in the meshes of the pia 
mater. 

THE SPINAL CORD. 

Hmmorrhage. — This is much less frequent than in the brain, but 
may occur either as capillary apoplexy or as larger apoplectic clots. 
Capillary haemorrhages, similar in appearance to those of the brain, may 
occur as the result of injury, or near areas of softening or tumors, or 
may accompany severe convulsions, as in tetanus. Apoplectic clots, 
which are comparatively rare in the spinal cord, are usually small, com- 
monly not more than one cm. in diameter, and are similar in their ap- 
pearances, and in the changes subsequent to their formation, to those of 
the brain. They are usually the result of injury; but may occur spon- 
taneously, probably in most cases as a result of inflammation, and are 
then most apt to occur in the gray matter. Sometimes, however, 
hemorrhagic foci are found in the spinal cord without traumatism or 
evidence of inflammatory change. 

INJURIES. 

The spinal cord may be compressed or lacerated by penetrating 
wounds, by fracture or dislocation of the vertebrae, or by concussion 
■without injury to the vertebrae. The spinal cord is found simply disin- 
tegrated, or there may be much haemorrhage and the disintegrated nerve 
tissue be mixed with blood. If life continue, the nerve elements may 
degenerate, Gluge's corpuscles and free fat-droplets may form; blood- 
pigment may be formed, and when inflammation supervenes, more or 
less pus may be intermingled with the degenerated detritus. There 
may be marked changes in the minute structure of the cord without any 
change being evident to the naked eye. 

SECONDARY DEGENERATIONS IN THE SPINAL CORD. 

When nerve fibres of certain parts of the brain and of the spinal cord 
are divided or destroyed from any cause, that portion of them which be- 
comes separated from its trophic centres degenerates. After a time — 
frequently two to four weeks — the medullary sheath and axis cylinder 
disintegrate, becoming granular and fatty. These products of degenera- 
tion maybe in part absorbed at once, or may collect in cells, forming the 
so-called compound granular corpuscles. After a still longer time — 
sometimes several months— the degenerated areas become gray in color, 



200 THE SPINAL COED. 

from the absorption of the degenerated myelin, harder, and somewhat 
shrunken. These changes are partly due to the formation of new con- 
nective tissue which takes the place of the degenerated nerve fibres. 

Since the affected portion of nerve tissue becomes gray or translucent 
after the myelin is broken down and absorbed, and the new connective 
tissue is formed, this is often called Gray Degeneration ; or as the de- 
generated areas are harder than normal, it is sometimes termed Sclerosis. 

Now, it is found that this secondary degeneration takes place in the 
direction in which the fibres conduct — in centripetal or sensory fibres, 
upward ; in centrifugal or motor fibres, downward. Thus, we have 
Descending Gray Degeneration (Descending Sclerosis), and Ascending 
Gray Degeneration (Ascending Sclerosis). 

Descending Gray Degeneration. — This change affects only the motor 
nerve fibres, and may reach but a short distance from the seat of lesion, 
or may extend for a long distance, depending upon whether the severed 




Fig. 97.— Descending Gray Degeneration. 
Section of cord in cervical region, showing secondary degeneration from softening in pons 
which had existed for at least six months. A, column of Turck on same side as brain lesion; B, 
pyramidal tract on opposite side. 

fibres run a short or long course before reaching their termination, i.e., 
passing into ganglionic centres. Lesions of the brain, such as embolic 
softenings and apoplectic clots, w 7 hich destroy or interrupt any of the 
motor nerve fibres originating in the central convolutions, may be fol- 
lowed by gray degeneration of the portion of the fibres situated periphe- 
rally to the lesion. These fibres pass through the corona radiata, anterior 
portion of the internal capsule, pes pedunculi, pons, and thence to the 
anterior pyramids, where most of them decussate and pass to the poste- 
rior part of the lateral columns of the opposite side. Those which do 
not decussate form a narrow band at the inner part of the anterior 
columns of the same side, constituting the columns of Turck. These 
fibres which convey motor impulses from the brain to the cord form 
a system called the pyramidal tract. There are also short motor fibres 
in the anterior columns, forming the so-called anterior root zones, 



THE SPINAL COED. 



201 



which maintain communications between different portions of the gray 
matter. 

Now, a lesion in the brain or medulla, destroying the continuity of 
the motor nerve fibres of the pyramidal tract, will be followed by areas 
of gray degeneration in the posterior part of the lateral column of the 
opposite side, and in a narrow band near the anterior longitudinal fis- 
sure of the same side (see Fig. 97). A lesion below the medulla, involving 
the fibres of the pyramidal tract, will be followed by degeneration of 
the fibres on the same side below the poiut of lesion. Lesions involv- 
ing the fibres of the anterior root zones will be followed by degenerations 
which extend but a short distance, since these fibres soon communicate 
with their centres in the gray matter. If a part only of the fibres in 
any of these regions are interrupted, the amount of degeneration is pro- 
portionately small. 

Ascending Gray Degeneration. — Any lesion interrupting the course 



c— m 




Ml 




4c— 



Fig. 98.— Ascending Gray Degeneration. 
Section of cord in cervical region, showing secondary degeneration from a tumor in the dorsal 
region of 18 to 20 months' duration. A, columns of Goll; B, pyramidal tract; C, columns of 
Gowers (antero-lateral ascending tract). Drawn from a specimen prepared by Dr. Ira Van Gieson. 

of the sensory nerve fibres in the cord is followed by degeneration of the 
central ends of the involved fibres, and increase of connective tissue 
about them. These fibres are in part situated in the posterior columns, 
and form communications between different parts of the gray matter— 
posterior root zones— and hence have not great length. Other sensory 
fibres are grouped in a narrow band near the posterior longitudinal fis- 
sure, forming the columns of Goll, while other sets, forming the so- called 
direct cerebellar tract and the columns of Gowers, are situated in the 
periphery of the lateral columns. 

A lesion of the cord involving the severance or destruction of these 
centripetal fibres will be followed by gray degeneration of the entire pos- 
terior columns, and the cerebellar tract, and the columns of Gowers for 
a short distance above the lesion. The fibres of the posterior root zone 
being short, however, the degeneration will, at a short distance above 
15 



202 THE SPINAL COED. 

the lesion, become limited to the columns of Groll, the direct cerebellar 
tract, and the columns of Gowers in the lateral columns (Fig. 98). The 
degeneration may be traced along the columns of Groll to the restiform 
bodies, and in the cerebellar tract to the cerebellum. Lesions in- 
volving the entire thickness of the cord will produce bilateral de- 
generations. 

It should be borne in mind, in looking for these secondary lesions, 
that they are not developed until considerable time has elapsed since the 
primary lesion, and that, when small areas are involved, they are 
usually inconspicuous. In any event, the lesions are apt to be more 
evident to the naked eye in specimens hardened in chromic fluids than 




Fig. 99.— Ascending Gray Degeneration. 
A small portion from edge of degenerated region of cord shown in Fig. 98, more highly magni- 
fied. A, normal nerve fibres; B, degenerated area. 

when fresh, and microscopical examination is often necessary for their 
recognition (Fig. 99). 

INFLAMMATION. 

Acute Myelitis. 

This lesion of the spinal cord, which is sometimes distinctly inflam- 
matory in character, and sometimes of a rather degenerative nature, is 
usually confined to a comparatively limited longitudinal extent of the 
cord, and hence is sometimes called transverse myelitis. When the 
cord is removed and laid upon the table, if the lesion is marked a flat- 
tening of the cord at its seat may be observed; or on passing the finger 
gently along the organ, the affected segment will be found softer than 
the rest of the cord. On making a section through the diseased portion, 
the nerve tissue may be white or red or yellowish or grayish; it may be 
quite firm, but is usually more or less softened and sometimes almost 
diffluent. 1 

Microscopical examination shows different appearances, depending 

1 It should be remembered that a mechanical injury to the cord in removal, such 
as crushing or bruising, may reduce the injured portion to a pulpy consistency and 
thus produce appearances somewhat similar to those of some forms of inflammatory 
softening. 



THE SPINAL COED. 



203 



upon the stage of the inflammatory or degenerative process. There may 
be much blood, or, if the lesion has existed for some time, blood pig- 
ment; also fragments of more or less degenerated nerve fibres and cells 
(Fig. 100), myelin droplets, free fat-granules, and larger and smaller cells 
filled with fat-granules (Gruge's corpuscles), pus cells, granular matter, 
neuroglia cells, and sometimes corpora amylacea. The various combina- 
tions of these elements give rise to the different gross appearances which 
the diseased part presents. In earlier stages of the lesion, the blood- 
vessels may be dilated, the nerve fibres and cells swollen; or the walls of 
the blood-vessels may be thickened or fatty. 

The lesion is apt to commence in the gray matter or at its edge, and 
then extend first laterally and afterwards upward and downward. 

In a certain number of cases, the degenerated material may be ab- 
sorbed and a cicatrix or cyst formed. In the least extensive forms of 
the lesion, there is apparently a regeneration of the nerve fibres and a 
restoration of the functions of the cord. 




Fig. 100.— Degenerated Tissue prom Acute Myelitis. 



Secondary gray degeneration, both ascending and descending, may 
occur in this form of myelitis, varying in extent according to the size of 
the primary lesion. 

Acute disseminated Myelitis runs a rapid course, and proves fatal in 
a short time. The inflammation involves nearly the whole length of the 
cord, but is more intense in some places than in others. The cord is 
swollen and congested, it is infiltrated with pus cells, the connective-tis- 
sue framework is swollen, and the nerve elements are degenerated. 

Poliomyelitis anterior (Myelitis of the anterior horns).— -This name 
is applied to a group of cases which are characterized by clinical symp- 
toms indicating changes in the anterior gray cornua. The disease occurs 
both in children and in adults, and varies in the severity, acuteness, and 
duration of its symptoms. In many cases, there is complete recovery, 
and then we must suppose that the changes in the nervous tissue were 
not destructive in their character. In other cases, the symptoms are 
more permanent, indicating a destructive lesion. From the autopsies 



204 



THE SPINAL CORD. 



so far recorded, we learn that the lesion is most frequent at the lumbar 
and cervical enlargements of the cord, but may occur anywhere, and is 




Fig. 101.— Poliomyelitis anterior. 
Showing portion of Fig. 102 at edge of affected area, more highly magnified. A, normal gan- 
glion cells surrounded by nerve fibres; B, degenerated ganglion cells; C, granular masses at place 
of ganglion cells; D, small cavity containing fluid. 

often in^scattered patches. There is degeneration, shrinkage, pigmen- 
tation, and atrophy of the ganglion cells in the anterior gray cornua 














Fig. 102.— Poliomyelitis anterior. 
Showing degenerated area in anterior cornua, with atrophy of gray matter. A, atrophic region 
CWeigert's haematoxylin stain). Specimen prepared by Dr. Ira Van Gieson. 

(Fig. 101). There may be an increase of connective tissue in the gray 
cornua and in the anterior and lateral columns. There may be degene- 



THE SPINAL COED. 



205 



ration and destruction of a considerable part of the anterior cornua; 
there may be atrophy of the anterior nerve roots. The cord may be con- 
siderably distorted as the result of the lesion (Fig. 102). 

Chronic Myelitis, 

Chronic Interstitial Myelitis. — Under this heading are embraced a 
variety of lesions which probably differ from one another somewhat in 
the nature of the changes involved, but more in the seat of the disease. 
We shall consider without special classification the most important 
forms. 

Chronic Transverse Myelitis. — In certain cases of pressure on the 
spinal cord from a tumor or from displacement of the bones of the ver- 



■:*?.. 








--ff^i 







Fig. 103.— Posterior Spinal, Sclerosis. Upper dorsal region. 

tebral column, etc., instead of becoming softened or undergoing acute 
inflammatory changes, the cord becomes the seat of a localized formation 
of new connective tissue, with consecutive atrophy of more or less of the 
nerve elements in the gray and white matter. The cord becomes in this 
way harder, and sometimes shrunken at the seat of lesion, and grayish 
in color. This change may be followed by ascending and descending 
gray degeneration. 

Multiple Sclerosis. — This lesion, similar in its nature to multiple 
sclerosis of the brain, and often occurring with it, seems to belong, like 
other chronic inflammations of the cord considered in this section, to the 
group of chronic interstitial inflammations. It consists in the formation, 
in more or less numerous, scattered, circumscribed areas, of new connec- 



206 



THE SPINAL COED. 



tive tissue, apparently derived from the neuroglia. The formation of 
new connective tissue is accompanied by degeneration and atrophy of the 
nerve fibres and ganglion cells. Whether the formation of new connec- 
tive tissue is primary and the atrophy of the nerve elements secondary, 
or vice versa, it is difficult to say. The new connective tissue consists of 
the characteristic branching neuroglia cells surrounded by a more or less 
dense network of fine fibrillar many if not most of which seem to be 
branches of the neuroglia cells. Corpora amylacea and sometimes fat- 
droplets, either free or contained in cells, maybe present in the sclerosed 
areas. 

The areas of sclerosis may involve both gray and white matter, and 
may be very small or large. If very small, or in early stages of forma- 
tion, they may not be recognizable by the naked eye, but when visible 




T*». 



Fig. 104.— Posterior Spinal Sclerosis. 



A portion of sclerosed area shown in Fig. 103, more highly magnified, a, new-formed connec- 
tive tissue; &, blood-vessels; c, nerve fibres; d, atrophied nerve fibres. 

they are grayish, translucent, and firmer than the surrounding tissue, 
and may or may not present a depressed surface; they sometimes project 
above the general level. The cause of this, as of other forms of so-called 
idiopathic interstitial myelitis, is very obscure. 

Posterior Spinal Sclerosis (Locomotor Ataxia). — This lesion consists 
essentially in a degeneration and atrophy of the nerve fibres and an in- 
crease of connective tissue in the posterior columns of the spinal cord 
(Fig. J 03). Not infrequently the posterior portion of the lateral columns, 
the posterior roots and cornua are also involved. Exceptionally a large 
part of the lateral columns is involved, and also the anterior cornua. The 
change usually commences in that portion of the posterior columns 
bordering on the posterior cornua, but may involve, as above stated, the 



THE SPINAL COED. 207 

adjacent parts. It is usually most marked in the lower dorsal and 
lumbar regions. The sclerosis may extend upward to the restiform 
bodies, but in the cervical region it is apt to be confined largely to the 
columns of G-oll, although there are exceptions to this. 

When the lesion is well developed, the pia mater over the affected 
area is usually thickened and adherent to the cord. In its early stages 
there may be no change evident to the naked eye; but when advanced, 
the posterior columns may appear somewhat depressed, and grayish and 
firmer than the rest of the cord. The microscopical appearances vary, 
depending upon the stage and extent of the lesion. The walls of the 
blood-vessels may be thickened; there is more or less new connective 
tissue consisting of neuroglia cells and very numerous interlacing, deli- 
cate fibrils. There may be numerous corpora amylacea and fat-granules, 
either free or collected in cells. The nerve fibres may be numerous, but 
separated more or less widely by the new connective tissue, or they may 
be very few in number and irregularly scattered through the new tissue 
(Fig. 104). The atrophy may involve the fibres of the posterior nerve 
roots and cornua, and even the ganglion cells of the latter. 

According to the recent researches of Lisauer, 1 the columns of Clarke 
in the dorsal region show in this disease a very constant and marked 
diminution in the number of delicate fibrils which under normal condi- 
tions surround the ganglion cells. 

In the. rare cases in which the sclerosis extends to the lateral columns 
and to the anterior cornua, the minute characters of the lesions are the 
same. 

There are other less important and less well understood forms of scle- 
rosis of the white matter and degenerative or inflammatory changes in 
the gray matter of the cord; but, so far as we know, the character of the 
lesions is essentially the same as those above described, except in their 
distribution. They are associated either with paralysis or changes in 
the muscles, and the secondary changes are for the most part better 
known than the primary alterations in the cord. Such lesions, which 
the scope of this book does not permit us to enter into, are lateral scle- 
rosis, peripheral sclerosis, the lesions involving muscular atrophy, etc. 

Solitary tubercles and gummata may occur in the spinal cord, but 
are not common. Cysts may occur as a result of softening, or from un- 
known causes. Sometimes very long, narrow canals are found in the 
spinal cord, even reaching nearly its whole length. Some of these are 
evidently the dilated central canal, as they are lined with epithelium. 
Others, however, have been found behind the central canal, and their 
mode of origin is unknown. 

Tumors. — Tumors of the spinal cord are not very common, much less 

1 Fortschritte der Medicin, Bd. ii., No. 4, 1884. 



208 



THE SPINAL COKD. 



so than tumors of the meninges. Fibromata, gliomata, sarcomata, glio- 
sarcomata. and neuromata have been described as primary tumors. 
Carcinomata, as secondary tumors, may occur. Tumors of the men- 
inges are apt to secondarily involve the cord. 

SYEINGOMYELIA. 

This lesion of the spinal cord consists of the formation of gliomatous 
or glioma-sarcomatous tissue in the vicinity of the central canal, and its 
subsequent partial disintegration with the formation of one or more cavi- 
ties within the substance of the cord (Fig. 105). These cavities, which 
are filled with fluid, vary greatly in size, shape, and extent, and while 
usually situated in the central region of the cord, they may involve the 
anterior and posterior cornua and invade the posterior columns. There 
may be two communicating cavities, and these may, but usually do not, 



— G 




Fig. 105.— Syringomyelia. 
Transverse section of cord. A, white substance of cord, distended by tumor; B, B, distorted 
and atrophied gray substance of anterior cornua; C, tumor mass (glio -sarcoma) ; D, cavity in cord. 
Drawn from specimen prepared by Dr. Van Gieson. 



open into the central canal. The longitudinal extent of these cavities 
varies greatly. The lower cervical and upper dorsal regions are most 
frequently involved. The cavity is usually lined with tissue somewhat 
denser than that which makes up the bulk of the tumor. The glio- 
matous or glio-sarcomatous tissue, which forms the basis of the lesion in 
syringomyelia, probably originates from the layer of neuroglia which 
surrounds or extends away from the central canal. 

Syringomyelia is frequently mistakeu for hydromyelia (see below), 
which is a congenital malformation, and in which the longitudinal cavity 
in the cord is at some period lined with epithelial cells. 

There seems, furthermore, to be a class of lesions of the cord, usually 
classed as syringomyelia, in which cavities of various forms coexist with 
a tumor in the vicinitv of the central canal. But these cavities do not 



THE SPINAL CORD. 



209 



appear to be formed by a breaking-down of the tumor tissue, but in some 
other way as yet little understood. 

Altogether the limitations of the term syringomyelia are somewhat 
indefinite, and will no doubt remain so until we possess fuller knowledge 
of the genesis and structure of the neuroglia tissue of the spinal cord. 

MALFORMATIONS. 

The spinal cord may be double either in circumscribed portions or 
over a large part of its extent. It may be unusually long or short, or it 
may be absent altogether {amyelia). This usually occurs with anence- 
phalia. Under these conditions a long connective-tissue sac, filled w T ith 
more or less fluid, may occupy the spinal canal. 

Hydromyelia {Hydr or rhachis interna). — This abnormality consists in 
the dilatation of the central canal of the spinal cord by fluid (Fig. 106). 




Fig. 106.— Hydromyelia. 
In the section from which this drawing was made, the epithelial cells surrounding the dilated 
central canal were well preserved. 

This may be moderate, or so extreme that but little of the substance of 
the cord is left as a thin shell around the central cavity. When they 
have not been destroyed by atrophy, epithelial cells may be found lining 
the cavity. 

Hydr or rhachis externa. — In this lesion there is an accumulation of 
fluid between the meninges of the cord, causing more or less atrophy of 
the latter. 

Hydromyelocele— Spina bifida. — In the majority of cases, hydrorrha- 
chis is accompanied by a more or less complete lack of closure of the 
spinal canal posteriorly, so that the collections of fluid within may pouch 
outward through the opening, in the form of a sac. The sac may be 
covered by skin, or this may be absent, either from the beginning or as 
a result of thinning and rupture. The walls of the sac may consist of 



210 THE SPINAL CORD, 

the dura mater and pia mater, or, in cases of hydrorrhachis externa, of 
the dura mater alone; when both are present, they are usually more or 
less fused together. Inside of the membranes of the sac there may be a 
shell of distended nerve tissue of the cord, or the spinal cord may be 
split posteriorly and the sides crowded sideways; or there maybe a rudi- 
mentary fragment of the cord suspended in the sac or attached to the 
walls; or the cord may be but little changed and remain inside the spinal 
canal. The openings in the spinal canal may be due to the complete or 
partial absence of the vertebral arches, or more rarely the sac may pro- 
trude through openings between the completely formed arches. Spina 
bifida most frequently occurs m the lumbar and sacral regions, but it 
may occur in the dorsal or cervical regions; or the canal may be open 
over its entire length. Very rarely it is open on the anterior surface. 
The protruding sac may be very small or as large as a child's head. The 
fluid in the sac is usually clear, but may be turbid from flocculi of de- 
generated nerve tissue. 

THE PERIPHERAL NERVES. 

Changes in Nerves after Division. — When nerves are divided or a 
portion destroyed by injury, the nutrition of certain parts of the fibres 
is interfered with, apparently because of their separation from their 
trophic centres, and they suffer degeneration; but after a time, if the 
conditions be favorable, they may undergo regeneration and restitution 
of function. The degeneration not only affects the entire severed por- 
tion, but it occurs at nearly the same time in all parts. The degeneration 
consists in the breaking up of the medullary sheaths into variously shaped 
droplets, and the decomposition of these, with the formation of fat, 
which may remain for some time either free or inclosed in cells, and 
finally be absorbed (see Fig. 107). The axis cylinder, too, is, in many 
cases at least, more or less completely destroyed. The neurilemma and 
its nuclei do not seem usually to undergo degeneration, but may persist 
and take part in the regeneration of the nerve when restitution occurs. 

After a variable time, if the conditions are favorable, the divided 
ends of the nerve may be united and a regeneration or new formation of 
nerves in or about the severed portions may occur, so that the function 
may be resumed. Considerable time is required, frequently months, for 
the completion of the regenerative process. Degeneration of the nerves 
not only follows mechanical injuries, such as incision, crushing or 
tearing, and compression, as from a tumor or dislocation of the bones, 
but it may result from disease of the special nerve centres with which 
the nerves communicate, or from inflammation of the nerves themselves. 

Acute Exudative Neuritis. — Primary acute inflammation of the 
nerves may occur as the result of injury, or it may be secondary to an 



THE SPINAL COED. 211 

inflammatory process in its vicinity, although, owing to the dense 
lamellar sheaths and the special blood-supply, the nerve trunks may 
escape participation in even very severe inflammatory processes in sur- 
rounding tissues. The inflamed nerve may be red and swollen and infil- 
trated with serum and pus cells. The process may undergo resolution 
or terminate in gangrene and destruction of the nerve, or it may become 
chronic and result in the formation of new connective tissue. 

Degeneration and regeneration of the nerve fibres, similar to those 
above described as following division of nerve trunks, may occur in acute 
neuritis. 

Chronic Interstitial Neuritis. — This is essentially a chronic intersti- 
tial inflammation resulting in an increase of connective tissue in the 
nerve sheath and intrafascicular bands. As a result of this, the nerve 
fibres undergo atrophy from pressure; the medullary sheath, and finally 
the axis cylinder, being, in more or less of the fibres, partially or com- 
pletely destroyed. 




Fig. 107.— Multiple Neuritis. 
.From a case of alcoholic poisoning. Specimen stained with osmic acid. The broken-down 
medullary sheath and fat-droplets are stained deep black. 

Multiple Neuritis. — Under a variety of conditions, such as exposure 
to cold and wet, over-exertion, poisoning by alcohol, arsenic, lead, etc., 
and in connection with the acute infectious diseases, a degeneration of 
the nerve fibres in various parts of the body may occur, which may be 
accompanied with or followed by proliferative changes in the neurilemma 
cells (Fig. 107). Regeneration of the affected nerve fibres may occur 
under these conditions, as after experimental division of the nerves, 
leading to their restitution. 1 In some 'forms of multiple neuritis, the 
inflammation is exudative in character, and new cells of various forms 
are found within and between the nerve fibres. The exact part which 
the neurilemma and other intrafascicular cells play in the inflammatory 
and regenerative changes of nerves is not yet very fully made out. 

Syphilitic and Tubercular Inflammation of the nerves is not common 
except at their central ends, in connection with similar inflammations 
of the meninges, or when they are secondarily involved in connection 
with these inflammations in neighboring tissues. 

Consult Starr, "Multiple Neuritis." The Middleton Goldsmith Lecture for 
1887. Trans. New York Pathological Society, 1887, page 1. 



212 THE SPINAL COED. 

Leprous Inflammation. — This consists in the formation within the 
nerve of masses of new-formed tissue somewhat resembling granulation 
tissue, in whose cells multitudes of characteristic bacilli are uniformly 
found (see Leprosy). It constitutes the variety of leprosy known as 
lepra ancesthetica. 

Tumors. — The tumors of the nerves are such as consist largely of 
or contain new-formed nerve tissue — true neuromata ; and the so-called 
false neuromata (Figs. 63 and 64), which are for the most part fibro- 
mata or myxomata of the connective tissue of the nerve. Myxo-sarco- 
mata are less common, and primary sarcomata rare. The nerves may 
be secondarily involved in sarcomata or carcinomata, though not infre- 
quently nerves pass through these tumors without being in the least 
involved in their peculiar structure. 

METHODS OF PREPARATION OF NERVE TISSUE FOR MICROSCOPICAL 

STUDY. 

The general methods of hardening have been already given on page 
15. For minute study, there is no one method of staining and mounting 
upon which we can rely exclusively for the study of all lesions. A pre- 
liminary examination of areas of inflammatory softening, or of the dis- 
integrated tissue in apoplectic clots, or of the new-formed tissue in chronic 
hemorrhagic pachymeningitis interna, may be made by teasing portions 
of the affected tissues in one-half-per-cent salt solution. Or the tissues 
in these lesions, or in any others in which fatty degeneration is sus- 
pected, may be placed for twenty-four hours in one-per-cent aqueous 
solution of osmic acid, and then washed and teased in glycerin. In this 
way, the myelin and the fat will be stained brown or black. Secondary 
and other degenerations of meduliated nerves may be studied by soaking 
the nerves for twenty-four hours in one-per cent solution of osmic acid, 
and then staining with picro-carmine and teasing and mounting in gly- 
cerin. Suppurative inflammation of the central nervous system and the 
membranes, or the connective-tissue changes in general, may be studied 
in sections from the tissues hardened in Muller's fluid and alcohol, 
stained double with hematoxylin and eosin (see page 47), and mounted 
in Canada balsam. 

A very useful method of staining sections of nerve tissue, especially 
of the brain and cord, is that known as Weigert's hematoxylin method. 
The tissue is first well hardened in Muller's fluid. 

Blocks of the hardened tissue are imbedded in celloidin, and sections 
made in the usual way. The sections are first soaked for twenty-four 
hours in a saturated aqueous solution of neutral cupric acetate diluted 
with an equal bulk of water. They are now transferred to the hema- 
toxylin solution, made as follows: 



THE SPINAL COED. 213 

Hematoxylin Crystals 1 gm. 

Alcohol, 97 per cent 10 c.c. 

Water , 90 " 

Sat. Aqueous Sol. Lithium Carbonate 1 " 

In this solution the sections remain for two hours. (If the finer 
fibres of the cerebral cortex are to be brought out, the sections must re- 
main for twenty-four hours in the hematoxylin solution.) The sections 
are now thoroughly washed in two or three waters, and then rinsed in 
alcohol and transferred to the bleaching solution, composed as follows: 

Potassium Eerri cyanide 2.5 gm. 

Sodium Biborate 2. " 

Water 200 c.c. 

In this fluid the sections discharge a brownish color, and they re- 
main in it until the gray matter has a distinct yellow color and the 
white matter is bluish black. The time required to produce this effect 
varies considerably, but is usually from one-half an hour to an hour. The 
sections are now washed, dehydrated with alcohol, cleared up in oil of 
cloves or oil of origanum, and mounted in balsam. The sections may 
be stained in alum carmine before dehydration, to bring out the nuclei. 

In sections stained by this method, the gray matter, connective- 
tissue elements, and ganglion cells have a yellow or yellowish-brown 
color, the axis cylinders are uncolored or have a slight yellowish tint, 
while the medullary sheaths are bluish black or black (see Fig. 101). 

To demonstrate the presence of miliary aneurisms in or about apo- 
plectic clots, it is usually necessary to macerate the brain tissue in water 
until the nerve elements disintegrate, and they may then be washed 
away under a stream of water, leaving the blood-vessels with their 
aneurisms exposed. 



THE KESPIBATORY SYSTEM. 



THE LARYNX AND TRACHEA. 
MALFOEMATIONS. 

The larynx and trachea may be entirely absent in acephalic monsters. 
The larynx may be abnormally large or small. The epiglottis also may 
be too large or too small, or may be cleft. There may be communica- 
tions between the trachea and the oesophagus, and then the pharynx 
generally ends in a cul-de-sac, and the oesophagus opens into the trachea. 
There may be imperfect closure of the original branchial arches, so that 
there are fissures in the skin leading into fistulas which open into the 
pharynx or trachea. The fissure in the skin is small, and is situated 
about an inch above the sterno-clavicular articulation, usually on one or 
both sides, more rarely in the middle line. Individual cartilages, as the 
epiglottis, or one or more rings of the trachea, may be absent, or there 
may be supernumerary rings. The trachea may divide into three main 
bronchi instead of two, and in that case two bronchi are given off to the 
right lung and one to the left. The trachea may be on the left side of 
the oesophagus, or behind it. 

INFLAMMATION. 

Acute Catarrhal Laryngitis. — This occurs as an idiopathic inflam- 
mation, as a complication of the exanthemata and the infectious diseases, 
and is produced by the inhalation of irritating vapors and of hot steam 
and smoke. The inflammation varies in its intensity in different cases. 
The mucous membrane is at first congested, swollen, and dry; then the 
mucous glands become more active and an increased quantity of mucus 
is produced. There is an increase in the desquamation of the superficial 
epithelial cells, and in the production of the deep cells. A. few pus cells 
are found in the mucus and in the stroma of the mucous membrane. 
For some reason inflammation of the larynx is frequently attended with 
spasm of its muscles, thus producing attacks of suffocation. In severe 
cases, oedema of the glottis may be developed. 

After death, the congestion of the mucous membrane frequently dis- 
appears altogether. 



THE RESPIRATORY SYSTEM. 215 

Chronic Catarrhal Laryngitis.— -The surface of the mucous mem- 
brane is dry or coated with muco-pus. The epithelium is thickened in 
some places, thinned in others, or in places entirely destroyed. The 
stroma is somewhat infiltrated with cells, diffusely thickened, or forming 
little papillary hypertrophies, or thinned, or necrotic and ulcerated (Fig. 
108). 

The mucous glands are swollen and prominent. The inflammation 
may extend to the perichondrium of the cartilages, and thus cause their 
necrosis. The most severe forms of chronic laryngitis are those associ- 
ated with pulmonary phthisis. 

Croupous Laryngitis occurs most frequently as one of the lesions of 






Fig. 108.— An Ulcer of the Larynx in Chronic Catarrhal Laryngitis, x 850 and reduced. 

diphtheria; it complicates the exanthemata and the infectious diseases. 
It is produced by the inhalation of irritating gases, hot steam or smoke, 
and by the introduction of foreign bodies. 

The mucous membrane is swollen and congested. Its surface is 
coated with fibrin and pus, and its stroma is infiltrated with fibrin and 
pus. The epithelial cells undergo coagulation necrosis. It is not often 
that there is necrosis of the deeper tissues. 

Syphilitic Laryngitis. — Syphilis often causes laryngitis. The in- 
flammation may have the ordinary characters of an acute or chronic 
catarrhal inflammation, or it is a productive inflammation with the for- 
mation of new tissue in the stroma of the mucous membrane. This new 



216 THE RESPIRATORY SYSTEM. 

tissue is principally composed of small cells, which often degenerate and 
die. In this way, the mucous membrane of the larynx and the tissues 
beneath are thickened in some places and destroyed in others, these 
changes being especially marked in the upper portion of the larynx. If 
the perichondrium is involved by these changes, there may be necrosis 
of the laryngeal cartilages. 

Tubercular Laryngitis in its simplest form consists of a catarrhal 
inflammation, a growth of new cells in the stroma, and the formation of 
tubercle granula in the stroma without necrosis. The mucous membrane 
is thickened; it is coated with a layer of mucus, pus, and desquamated 
epithelium. From the epithelial layer outward, the stroma is infil- 
trated with cells and with tubercle granula (Fig. 109). 






\i 6 " ■■'■". : .. ' v -'"'-''. ■'.'•'/■■" -'■ v* ■■>%>■-;- ^ "•'■;■■"■':■ '..'-' : 4 :: i'*-s : ;7'-~ '^?^\^-'':^^: : ^Cl 
Fig. 109.— Tubercular Laryngitis. 

When there are added to the production of tubercle tissue an exces- 
sive formation of cells and a tendency to necrosis, the conditions be- 
come much more serious and complicated. The catarrhal inflammation 
is intense, with the production of large quantities of pus and mucus. 
The necrosis results in the formation of ulcers of different sizes and 
shapes; the inflammation and necrosis extend from the mucous mem- 
brane to the wall of the larynx. The epiglottis, the vocal cords, and 
the adjacent mucous membrane are coated with muco-pus; their sur- 
faces are ragged and irregular. In places the mucous membrane is 
destroyed, so that ulcers are formed ; in places it is thickened and in- 
filtrated with cells and tubercular tissue; in places it is necrotic. In 
the most severe cases, the entire thickness of the wall of the larynx, with 
its cartilages, is involved. 



THE RESPIRATORY SYSTEM. 217 

(Edema of the Glottis is the name given to serous infiltrations of the 
mucous membrane of the upper part of the larynx. The swelling is 
most marked on the posterior wall of the epiglottis, in the aryepiglot- 
tidean ligaments and the false vocal cords. In these places, the oedema 
of the stroma of the mucous membrane may be sufficient to close the 
larynx. 

Acute oedema is due to an inflammatory exudation of serum, and 
accompanies inflammations of the pharynx, larynx, and neck. 

Chronic oedema is of dropsical character and is caused by disease of 
the heart, pulmonary emphysema, and compression of the veins of the 
neck. 

Acute Suppurative Inflammation may attack the posterior surface of 
the epiglottis and the aryepiglottidean ligaments. The stroma of the 
mucous membrane is swollen and infiltrated with serum and pus. Ab- 
scesses may be formed in the stroma, which rupture internally, or ex- 
tend outward into the neck, or into the wall of the pharynx or of the 
oesophagus. Suppurative inflammation may accompany catarrhal, 
crupous, tubercular, and syphilitic laryngitis, inflammations and in- 
juries of the pharynx and tonsils; it may complicate typhoid fever and 
the other infectious diseases. 

TUMORS. 

■ Retention cysts of the mucous glands of the larynx may reach such a 
size as to form sacs projecting into its cavity. 

Papilloma is the most frequent form of tumor of the larynx. The 
tumors grow most frequently from the vocal cords. They consist of a 
connective-tissue stroma arranged so as to form papillae covered with 
epithelium. 

Fibromata, lipomata, myxomata, and angiomata are occasionally met 
with. 

Chondromata grow from the normal cartilages and are usually mul- 
tiple and sessile. They may project into the cavity of the larynx. 

Sarcomata of the larynx have been seen in a considerable number of 
cases. They occur both in children and in adults. They are composed 
of fusiform or round cells, with a stroma which varies in quantity in the 
different cases. 

Carcinomata may invade the larynx from the tongue or the pharynx, 
or may originate in it. They are composed of flat epithelial cells packed 
together in the usual way. 

In the trachea, tumors are of rare occurrence, but occasional exam- 
ples of growths similar to those in the larynx have been met with. 
16 



218 THE RESPIRATORY SYSTEM. 



THE PLEURA. 



HYDROTHOKAX. 



Non-inflammatory accumulations of clear serum in the pleural cavi- 
ties are of frequent occurrence. They are produced by the same causes 
which effect dropsy in other parts of the body — lesions of the heart, 
liver, and kidneys, and changes in the circulation and in the composi- 
tion of the blood. 

If the amount of serum is small, it is of little consequence; if it is 
large, it may compress the lower lobes of the lungs and interfere with 
respiration. 

There may be changes in the endothelium of the parietal pleura. 
Instead of the regular endothelium, large and small flat cells of irregular 
shape are found. 

HEMORRHAGE. 

Extravasations of blood in the substance of the pleura are found in 
persons who have died after suffering from the infectious diseases; and 
as the result of injuries to the wall of the thorax. 

Blood in large quantity in the pleural cavities is found after rupture 
of aneurisms of the heart and pericardium. 

Bloody serum in the pleural cavities is not often found with ordinary 
pleurisy. But with tubercular pleurisy and traumatic pleurisy it is not 
infrequently present. 

INFLAMMATION. 

The inflammations of the pleura are all spoken of by the common 
name of pleurisy. 

All the different inflammations of the lung are capable of being ac- 
companied by pleurisies, which begin in the pulmonary pleura and ex- 
tend to the costal. 

Besides these, however, there are many pleurisies which belong pri- 
marily to the costal pleura and extend from there to the pulmonary 
pleura. 

Such pleurisies occur as idiopathic inflammations, as complications of 
various diseases, as the result of injuries, or are produced by the inflam- 
mation of adjacent parts. 

We can distinguish: 

I. Pleurisy with the production of fibrin. 
II. Pleurisy with the production of fibrin and serum. 

III. Pleurisy with the production of fibrin, serum, and pus. 

IV. Chronic pleurisy with the formation of adhesions. 
V. Tubercular pleurisy. 

All the varieties of pleurisy can best be studied in the lesions which 



THE RESPIRATORY SYSTEM. 219 

are developed in and on the costal pleura. The lesions can be observed 
in the human subject, and can be produced artificially in the lower ani- 
mals. It is in these artificial pleurisies especially that we are able to see 
the early changes produced by the inflammation, and to watch the pro- 
cess step by step. 

The free surface of the costal pleura is covered with a single layer of 
flat cells — the endothelium. The pleura itself is formed of planes of 
connective tissue, reinforced by elastic fibres. Connective-tissue cells 
with large bodies and branching processes are present in considerable 
numbers, being most abundant in the layers beneath the endothelium. In 
the connective tissue are imbedded blood-vessels, lymphatics, and nerves. 

/. Pleurisy with the Production of Fibrin — Dry Pleurisy — Acute 

Pleurisy. 

This form of pleurisy is apt to involve circumscribed areas of the 
costal, mediastinal, diaphragmatic, or pulmonary pleura, less frequently 
the entire pleura of one side of the chest. While the inflammation is 
going on, the affected portion of pleura is coated with fibrin, the surface 
of the opposite portion of pleura is coated in the same way, and bands of 
fibrin join the two together. After the inflammation has run its course, 
we find the affected portion of pleura thickened by the formation of new 
connective tissue, while bands of connective tissue extend between the 
opposed pleural surfaces. 

As an exceptional condition there is inflammation of the entire pleura 
of one side, with the production of such an enormous amount of fibrin 
as to compress the lung and cause death. 

27. Pleurisy with the Production of Fibrin and Serum — Pleurisy with 
Effusion — Subacute Pleurisy. 

This is the most common form of pleurisy. As a rule, it involves the 
greater part of the pleura of one side of the chest. Sometimes, however, 
the pleura of both sides of the chest is involved, and then the pericardium 
also is often inflamed. 

While the inflammation is in progress, the surface of the affected 
pleura is coated with fibrin, and bands of fibrin stretch between the 
parietal and pulmonary pleura. In the pleural cavity is serum in vari- 
able quantity. This serum is clear, or turbid from the presence of pus 
cells and flocculi of fibriu. The lung is compressed in different degrees 
and positions, according to the quantity of the serum and the character 
of the adhesions. 

If the patients recover, the serum is absorbed, the fibrin disappears, 
and there are left behind connective-tissue thickenings of the pleura and 
adhesions. 



220 THE RESPIRATORY SYSTEM. 

These two forms of pleurisy, although different in their clinical his- 
tories, are yet anatomically essentially the same. In both of them we 
find a regular sequence of changes. First, the production of fibrin and 
a few pus cells, either with or without serum. Second, a gradual ab- 
sorption of the serum and fibrin. Lastly, the formation of permanent 
new connective tissue in the form of adhesions or of thickenings of the 
pleura. Throughout the whole process the tissue of the pleura is but 
little changed; the products of inflammation, although they originate in 
the tissue of the pleura, do not infiltrate it, but make their way to its 
surface, there accumulate, and there undergo their different changes. 
Variations from the regular course of the inflammation are effected by 



' \ f , 



f\ 



Ihhr»: *.jb «> 



'■-J' 




Fig. 110.— An Artificial Pleurisy in the Dog op Twenty-four Hours 1 Duration, x 750 and 

reduced- 
Swelling and growth of connective-tissue cells in the pleura. 

the excessive formation either of the fibrin, the pus, or the serum, and 
by the manner in which these inflammatory products are absorbed. 

If we endeavor to follow out the successive changes by which the 
fibrin, pus, and serum make their appearance and then disappear, and the 
way in which permanent new connective tissue takes their place, we en- 
counter several difficulties. It is impossible to obtain autopsies which 
will give the lesions belonging to each successive day of the disease; the 
pleura does not really show well if the patient has been dead more than 
two or three hours before the autopsy; and in most cases the inflamma- 
tion is too intense, its products are too abundant, to be easily studied. 

To obviate these difficulties we must resort to the lower animals. 



THE RESPIRATORY SYSTEM. 



221 



By injecting a solution of chloride of zinc into the pleural cavities of 
dogs, we can excite pleurisies exactly resembling those which we see in 
the human subject. By varying the amount of fluid injected, we can 
obtain pleurisies of different degrees of intensity. By using a number 
of animals, we can observe the course of the inflammation from hour to 
hour, and from day to day. 

In such an artificial pleurisy, the first change is congestion. The 











Fig. 111. 



-Artificial Pleurisy in the Dog on the Fifth Day, x 750 and reduced. 
The layer of new tissue on the surface of the pleura. 



pleura is of a uniform bright red color, its surface moist and shining* 
There is as yet no serum and no fibrin. Already, however, the endo- 
thelial cells have fallen ofT in patches, the superficial connective-tissue 
cells are swollen and increased .in number, and a few pus cells are present. 
These are all the changes for from half an hour to fix hours after the 
irritant has been applied to the pleura. 

The next step in the inflammatory process is the production of 
serum and fibrin. The serum collects in the bottom of the pleural 



222 THE RESPIRATORY SYSTEM. 

cavity,, the fibrin coats the pleura. As the fibrin is produced the pleura 
loses its natural moist and shining appearance. The fibrin appears first 
in the form of little granules, knobs, and threads between the edges of 
the endothelial cells and overlying them. A few pus cells are entangled 
in the fibrin and infiltrated in the superficial layers of the pleura. The 
swelling and new growth of the connective-tissue cells are now well 
marked. The bodies of the branching cells are swollen, and small poly- 
gonal, nucleated cells, arranged in rows between the fibres of the base- 
ment substance, make their appearance. By the end of twenty-four 
hours these changes are fully developed (Fig. 110). 

After this the production of fibrin, serum, and new connective- 
tissue cells continues, and by the third or fourth day the new connec- 
tive-tissue cells are present, not only in the superficial layers of the 
pleura, but also in the layer of fibrin coating its surface and forming 
adhesions. 

By the fourth or fifth day, the cells in the fibrin are still more 
numerous; blood-vessels make their appearance, which can be injected 
from the arteries of the pleura (Fig. 111). 

After this the serum is gradually absorbed. The layer of fibrin and 
cells on the surface of the pleura exhibits a constant decrease of fibrin 
and increase of cells, and becomes more intimately connected with the 
surface of the pleura. 

By the fourteenth day the fibrin has disappeared, and a basement 
substance has been formed between the cells. Of the new cells, the 
superficial ones are changed into endothelium, the deeper ones into 
branching cells. The changes in the adhesions between the pulmonary 
and costal pleura are the same as those in the layer of 'fibrin coating the 
costal pleura. 

The lesions of human pleurisy seem to be essentially the same as 
those of the artificial pleurisy just described. But the inflammatory 
products are formed in larger quantities, a much longer time is required 
for their absorption, and the formation of new connective tissue follows 
more slowly. 

In these forms of pleurisy, therefore, two distinct processes take 
place: 

1. The blood-vessels are congested, and through their walls transude 
the plasma of the blood and a few white blood-globules. 

2. The superficial connective-tissue cells are increased in size and 
number. 

The products of the first of these processes, the fibrin and serum, are 
regularly reabsorbed. 

The product of the second of these processes, the new connective- 
tissue cells, regularly increases until a layer of new connective tissue is 
formed. 



THE RESPIRATORY SYSTEM. 223 

The natural termination of such a pleurisy is the recovery of the 
patient, with thickenings of the pleura and adhesions. 

The irregular terminations are: The death of the patient, the pro- 
tracted existence of the fibrin and serum, and the change of the char- 
acter of the inflammation so that pus is produced. 

III. Pleurisy with the Production of Fibrin, Serum, and Pus — 

Empyema. 

This form of pleurisy may occur under several different .conditions. 

1. The inflammation is at the very outset of severe character, with 
the formation of pus. 

2. A pleurisy with the production of fibrin and serum, either 
gradually or suddenly, changes its character, and pus is formed. 

3. Phthisical areas of softening, or abscesses of the lung, abscesses in 
the wall of the thorax, or in the liver, or in the abdomen, rupture into a 
pleural cavity and set up an empyema. 

4. The inflammation may be not only purulent, but also gangrenous 
in character. The fluid in the pleural cavity, the fibrin and pus coating 
the pleura, and the pleura itself, may putrefy, with the proliferation of 
bacteria and the evolution of gases. This may take place either in a 
closed pleura or in one which has been opened. 

5. If there is an opening into a pleural cavity, either through the 
lung or through the wall of the thorax, there is air in the pleural cavity, 
in addition to the inflammatory products. Such a condition is called 
pyo-pneumothorax. 

In all these different cases, the pleural cavity is partly or completely 
filled with purulent fluid, and the lung is either compressed against the 
vertebral column or partly adherent to the chest wall. Sometimes, 
however, the purulent fluid is shut in by adhesion^, either between parts 
of the lung and the thoracic wall, or between the lung and the diaphragm, 
or between the lung and the pericardium, or between the lobes of the lung. 

The fluid in the pleural cavity is usually a thin, purulent serum, 
composed of serum, pus globules, endothelial cells, and pieces of fibrin. 
But sometimes this fluid is very thick and viscid. I 

In empyema in its earlier stages, the lesions are the same as those in 
pleurisy with effusion, with the addition of pus in the serum, the fibrin, 
and the superficial layers of the pleura. 

In children, the inflammation may remain in this condition for a 
long time, but in adults other changes in the pleura are soon developed. 

These changes consist in the growth of a large number of small poly- 
gonal and round cells, the basement substance is split up, and the pleura 
is changed into a tissue resembling granulation tissue. 

The pleura is thus considerably thickened. Its surface is coated 
with fibrin and pus, or is bare like the surface of an ulcer. 



224 THE RESPIRATORY SYSTEM. 

In this condition the pleura may remain for months or years; its 
inner layers formed of granulation tissue, its outer layers of dense con- 
nective tissue. 

Sometimes the cell growth is more active, necrotic changes are added, 
and so there is a conversion of portions of the pleura into pus. Such a 
suppuration may extend from the pleura to the fascise, the muscles, the 
skin, the diaphragm, or the lungs. Thus the pus may find an exit, 
through the wall of the thorax, into the peritoneal cavity or into the 
lungs. 

If the empyema becomes gangrenous, the pleural cavity contains foul 
gases, the purulent serum is dirty and stinking and swarms with bacte- 
ria. The fibrin coating the pleura is of green or brown color. Portions 
of the pleura itself may also become gangrenous. 

In old cases, the thickening of the pleura may reach an enormous 
degree, and it may become calcified. The perichondrium of the carti- 
lages and the periosteum of the ribs may become inflamed, with necrosis 
of the cartilages and ribs, or a production of new bone. 

Empyema is, therefore, a very much more serious lesion than the two 
forms of pleurisy just described. The lesions involve not merely the 
surface of the pleura, but its entire thickness. When the pleura has 
thus been converted into granulation tissue, it is hardly possible for it 
to return to a normal condition. 

It is important to remember that in children the changes in the 
pleura itself are less profound, and that in adults they become more. and 
more marked, according to the duration of the disease. 

IV. Chrome Pleurisy with the Formation of Adhesions. 

This form of pleurisy may follow one of the varieties of pleurisy just 
described, it may be associated with emphysema and chronic phthisis, or 
it may occur by itself. 

After death the pulmonary and costal pleura are found thickened 
and joined together by numerous adhesions. These changes may involve 
only a part or the whole of the pleura on one or both sides of the chest. 

The thickened pleura is covered with endothelial cells, which are in- 
creased in size and number; the connective-tissue cells in the pleura are 
also increased in number, and the blood-vessels are more numerous. 

The adhesions are formed of connective tissue resembling that of the 
costal pleura, containing blood-vessels and covered with endothelium. 

V. Tubercular Pleurisy. 

In acute general tuberculosis, miliary tubercles are often present in 
the pleura. In acute and chronic phthisis, besides the fibrin, pus, se- 
rum, and new connective tissue so often produced, there may also be 
miliary tubercles, or larger, flat, cheesy nodules. 



THE RESPIRATORY SYSTEM. 



225 



There are, however, cases of tubercular pleurisy which have the 
characters of a local tubercular inflammation. Tubercles are either ab- 
sent altogether from the rest of the body, or of secondary importance to 
the pleurisy. 

This form of pleurisy involves the pleura of one side of the thorax 
only. It may be rapidly developed, the patient dying at the end of two 
weeks; or it may continue for months. It seems to be very fatal. 



'■■sM^m-, 



>"-:-": -' 'r:\ : _~- 






&^^^-mmmM 



mm 



, 



















Fig. 112.— Tubercular Pleurisy, x 90 and reduced. 
Drawn from a vertical section of the costal pleura. 



The inflammation may be confined to the costal pleura, or may in- 
volve also the diaphragmatic and pulmonary pleura. The gross appear- 
ance of the lesion varies. 

1. The pleura is thickened, its surface is bare of fibrin; it is of a 
bright- red color from the congestion of the blood-vessels, and this red 
surface is mottled with white dots— the miliary tubercles. In the pleural 
cavity is bloody serum. 



226 THE RESPIRATORY SYSTEM. 

2. The pleura is thickened, it is thickly coated with fibrin, no tuber- 
cles are visible to the naked eye; the pleural cavity contains clear serum. 

3. The pleura is thickened and the pleural cavity contains purulent 
serum. 

In all the cases, the changes in the pleura itself are essentially the 
same. The thickened pleura is infiltrated with new connective-tissue 
cells. Scattered through its entire thickness are tubercle granula, 
either single or joined together by diffuse tubercle tissue (Fig. 112). The 
smaller blood-vessels show a growth of their endothelial cells. 

NEW GROWTHS. 

Fibroma. — Little white or pigmented fibromata of the size of a pin's 
head are often present in the pulmonary pleura. 

Larger fibrous tumors are formed in the deeper layers of the costal 
pleura, and project into the pleural cavity. They may become detached 
and are then found loose in the pleural cavity (Lebert). 

Lipoma. — Fatty tumors are formed beneath the costal pleura, and 
project into the pleural cavity (Lebert). 

Garcinomata, sarcomata, and lymphomata are usually secondary to 
similar tumors in other parts of the body. 

A peculiar form of primary new growth in the pleura has been de- 
scribed by several observers. 1 It is associated with a pleurisy with the 
production of fibrin and serum. There is a diffuse thickening of the 
costal pleura, or circumscribed nodules of different sizes. 

The new growth seems to begin in the lymphatics of the pleura, 
which are distended with flat, nucleated cells. 

I (Delafield) have seen two of these cases. The first case was a 
woman, fifty-three years old, who was ill with the symptoms of pleurisy 
with effusion, for four months. After death, the left pleural cavity was 
found to be full of bloody, purulent serum. The costal pleura was 
moderately thickened and coated with a layer of fibrin and pus. Beneath 
the fibrin and pus was a thin layer of granulation tissue. In this tissue 
and in the pleura were anastomosing tubules filled with flat, nucleated 
cells. The tubules looked like lymphatics. 

The second case was a man, sixty-three years old, who had the symp- 
toms of pleurisy with effusion, for four months. After death, the right 
pleural cavity was found half full of bloody serum. The costal, 
diaphragmatic, and pulmonary pleura were coated with fibrin, and con- 
tained numerous white nodules, some of them as large as a pigeon's egg. 
These nodules were formed of a connective-tissue stroma inclosing ir- 
regular spaces and tubules filled with flat, nucleated cells. 

1 Birch- EirschJ ? eld, "Path. Anat.," p. 768. E. Wagner, Arch. d. Heilkunde, xi. 
B. Schulz, Arch. d. Heilkunde, xv. Thierf elder, " Atl. d. path. Hist.," 4 Lief. 



THE RESPIRATORY SYSTEM. 227 

It is very difficult to class these tumors; whether to call them by the 
name of Carcinoma, Sarcoma, or Endothelioma is not easy to say. 

THE BRONCHI. 
INFLAMMATION". 

Acute Catarrhal Bronchitis is a disease of very common occurrence, 
but one which seldom proves fatal. Our knowledge of its lesions is de- 
rived from severe cases, from experiments on animals, from cases which 
are complicated by other diseases, and from the symptoms which we 
observe during life. 

The inflammation involves regularly the trachea and the larger and 



----- : V ; 1 
777" ~ : ;S'i>"^ -oi;>^.,-\- .i77^777"77 : ; --I-'-'-- - 1 , :>?•- %■'■■*:.-*■■ WZ-'^M 



d 



Fig. 113.— Acute Catarrhal Bronchitis, x 850 and reduced. 



medium- sized bronchi, less frequently the smaller bronchi also. As a 
rule, the bronchi in both lungs are equally affected. 

The first change seems to cousist in a congestion and swelling of the 
mucous membrane, with an arrest of the functions of the mucous 
glands. This is attended with pain over the chest, a feeling of oppres- 
sion, sometimes spasmodic dyspnoea, and a dry cough. After this, the 
mucous glands resume their functions with increased activity, the con- 
gestion diminishes, there is an increased desquamation of epithelium, an 
increased formation of the deeper epithelial cells, and a moderate 
emigration of white blood-cells. Sometimes the red blood-cells also 
escape from the vessels. The patient now has less pain and oppression, 



228 THE RESPIRATORY SYSTEM. 

the cough is accompanied with an expectoration of mucus mixed with 
epithelium, pus, and sometimes blood. 

After death, the only lesions visible are the increased amount of 
mucus, the growth of new epithelium, mucous degeneration of the epi- 
thelial cells,, a few pus cells infiltrating the stroma, and the general 
congestion of the mucous membrane. The whole process is a superficial 
one, not producing any changes in the walls of the bronchi beneath the 
mucous membrane (Fig. 113). 

When the inflammation involves the smaller bronchi also, they may 
be full of pus, but their walls are unchanged. 

The filling of the small bronchi may result in the collapse of the 
groups of air vesicles to which they lead, and thus are produced areas of 
atelectasis, which may be further changed by inflammatory processes. 

Chronic Catarrhal Bronchitis. — This form of bronchitis may be the 
sequel of one or more attacks of acute bronchitis. More frequently it is 
associated with emphysema, heart disease, interstitial pneumonia, phthi- 
sis, pleuritic adhesions, or the inhalation of irritating substances. 

There is, in most cases, a constant production of mucus, pus, and 
serum in considerable quantities, and these inflammatory products may 
have a very foul odor. Less frequently these products are very scanty 
— dry catarrh. 

In examining the bronchi in these cases after death, we are often 
struck by the want of proportion between the symptoms and the lesions. 
The same bronchi which during life were constantly producing large 
quantities of inflammatory products and injuring the patient's health, 
after death may be but little changed from the normal. In other cases, 
however, the lesions are more marked. 

The bronchi contain mucus and pus ; they may be congested; their 
walls are often trabeculated. The epithelium is deformed and desqua- 
mating, with a production of new cells in the deeper layers. The 
mucous glands are enlarged or atrophied. The connective-tissue stroma 
is thickened and infiltrated with cells. The coats of the arteries in the 
walls of the bronchi may be thickened. There may be cylindrical dila- 
tation of one or more bronchi. The muscular coat may be thickened 
or thinned. Very frequently the epithelial cells of the air vesicles and 
air passages are increased in size and number. 

Acute Croupous Bronchitis occurs as a lesion of diphtheria, as asso- 
ciated with croupous laryngitis, as the result of the inhalation of hot 
steam, with lobar pneumonia, and sometimes as an idiopathic disease. 

The bronchi are lined or filled with a mass of fibrin, pus, and 
desquamated epithelium. Fibrin and pus may also be found beneath 
the epithelium and infiltrated in the stroma. 

Chronic Croupous Bronchitis is attended with the formation in one 
or more bronchi of masses of fibrin which are expectorated by the patient 



THE RESPIRATORY SYSTEM. 229 

in the form of branching casts of the bronchi. The disease is a very 
chronic one, and is often associated with phthisis. After death, the 
bronchi are said to be found but little altered from the normal. 

Curschmann 1 has described under the name of "bronchiolitis ex- 
udativa" a form of bronchitis in which small threads and bands of 
gray or yellow, partly transparent, coagulated matter are formed in the 
small bronchi. Vierordt 2 has found similar formations in lobar pneu- 
monia. Leyden and Levi have found them in broncho-pneumonia. 

In different forms of bronchitis, especially in those associated with 
astbma, the exudation may contain small, octahedral bodies, probably 
composed of mucin. They are accidental formations, probably formed 
from cells, and may be found in the sputa. 

BRONCH1ECTASIA. 

Dilatation of the bronchi presents itself under three forms : the 
cylindrical, the fusiform, and the sacculated. 

The cylindrical dilatation is a uniform enlargement of one or more 
bronchi for a considerable part of their lengths. It is found in bronchi 
of every size, but most frequently in the medium sized. 

The fusiform dilatation is a mere variety of. the cylindrical. The 
bronchus is uniformly dilated for a short distance, and then resumes its 
natural size. Several such dilatations may be found in the same 
bronchus. 

The sacculated dilatations form the largest cavities. These cavities 
communicate with one side of the bronchus ; the peripheral portion of 
the bronchus may be obliterated. The bronchus leading to the cavity 
may be of normal size, or dilated, or stenosed, or even completely oblite- 
rated. Such sacculated dilatations may reach a very large size, and may 
communicate with each other. 

Any inflammatory process which involves the thickness of the wall 
of a bronchus seems to be capable of producing dilatation of that 
bronchus. 

In acute general bronchitis and broncho-pneumonia in children, 
cylindrical dilatation of a number of the medium-sized bronchi is often 
produced! 

In the persistent broncho-pneumonia of children, such dilatations 
reach a still greater development. 

In acute and chrouic phthisis, tubercular inflammation gives rise to 
sacculated dilatations, which expand with time and are made still larger 
by the destruction of the adjacent lung tissue. 

1 Deutsch. Arch. f. klin. Med., xxxii. 

2 Berl. klin. Wochensch., 1883. B. Levi, Zeitsch. f. klin. Med., ix. Leyden, 
Virch. Arch., Bd. 74. 



230 THE RESPIRATORY SYSTEM. 

Chronic bronchitis may lead to cylindrical or sacculated dilatations,, 
sometimes of great size. 

Occlusion of some of the bronchi, consolidation of portions of the 
lung, and extensive pleuritic adhesions, may also produce bronchiectasia. 

The walls of these dilatations may preserve the characters of the wall 
of the bronchus, more or less altered by inflammation (Fig. 114), or these 






I 



@S 



Fig. 114.— Section of the Wall of a Bronchiectasia, x 850 and reduced. 

characters may be altogether lost. The dilatations may contain mucus 
and pus, or they may be empty. 

NEW GROWTHS. 

Ossification of the w r alls of the bronchi is sometimes found. 

Lipoma in the submucous connective tissue has been described by 
Kokitansky. 

Carcinoma of the walls of the bronchi may occur as a secondary le- 
sion, but as a primary growth it is very rare. It may be formed in the 
large or small bronchi, follow the course of the bronchial tree, or extend 
to the lung tissue. 

Langhans 1 describes a primary carcinoma of the lower end of the 
trachea and the large bronchi in a man forty years old. The lower end 

1 Virchow's Arch., liii., p. 470. Virchow's Arch., Bd. 56, Bd. 85. Arch. d. Heil- 
kunde, xix. Prager med. Wochensch., 1883. Zeitsch. f. Heilkunde, v. 



THE RESPIRATORY SYSTEM. 231 

of the trachea and the large bronchi showed a general thickening of their 
walls, with flat tumors projecting inward. The new growth was com- 
posed of a stroma inclosing cavities filled with cells. The cells were 
small, nucleated, polygonal or cylindrical in shape, and packed closely 
together. Apparently the new T growth originated in the mucous glands. 

I (Delafield) have seen one case of new growth of the lower end of the 
trachea and large bronchi which I hardly know how to name. The pa- 
tient was a woman, twenty-seven years old, who suffered for seven months 
from cough, constantly increasing dyspnoea, and progressive emaciation. 
After death, the wall of the lower end of the trachea was found to be 
thickened. Its inner surface was studded with minute papillary out- 
growths. The epithelial cells were increased in size and number, and in 
some places were replaced for considerable spaces by a regular layer of 
pavement epithelium. The mucous glands were hypertrophied. The 
wall of the treachea from the basement membrane to the cartilages was 
thickened by new connective tissue. 

The walls of the large bronchi were very much thickened and their 
cavities nearly obliterated. The entire wall was thickened with new 
connective tissue. The epithelial layer was thickened, and in places re- 
placed by patches of pavement epithelium. The mucous glands were 
enlarged. 

Sarcomata of the walls of the bronchi occur as secondary growths, and 
as- prolongations of similar growths in the mediastinum. 

Primary sarcoma of the bronchi seems to be rare. 

Hesse ' describes a form of lympho-sarcoma, forming nodules around 
the bronchi, as of common occurrence among the miners in some cobalt 
and nickel mines. 

THE LUNGS. 
MALFORMATIONS. 

One or both lungs may be entirely wanting, or only partially devel- 
oped. In some of the cases with only one lung, the patients have grown 
up to adult life. 

A peculiar degeneration, by which the lung is converted into a num- 
ber of sacs containing air and serum, the sacs communicating with the 
bronchi, has been seen in a few instances. 

The lobes may be subdivided by deep fissures. An accessary lobe, 
separated from the lung, between the base of the left lung and the dia- 
phragm, has been described by Eokitansky. 

There may be hernia of the lung, with absence of part of the wall of 
the thorax. 

1 Arch. f. Heilkunde, xix., p. 160. 



232 THE RESPIRATORY SYSTEM. 

There may be transposition of the lungs, with similar changes in the 
position of the heart and the abdominal viscera. 

INJURIES — PERFORATIONS. 

Severe contusions of the thorax may produce rupture of the lungs, 
with extravasation of blood into the pleural cavities. 

The lungs may be wounded by a fractured rib and by penetrating 
weapons and projectiles. Such injuries often produce bleeding into the 
lung tissue and inflammatory changes. The lungs, however, exhibit a 
considerable degree of tolerance for such injuries, and the patients often 
recover. 

Collections of pus in the pleural cavities, the mediastinum, the liver, 
the spleen, the kidneys, and the peritoneal cavity may perforate the 
lungs. 

CONGESTION AND CEDEMA. 

These two conditions are regularly associated with each other in the 
lungs, although one or the other of them may preponderate in different 
cases. 

A moderate degree of congestion and oedema of the posterior portions 
of the lungs is often found as a result of post-mortem changes. 

In persons who have been comatose from any cause for some hours 
before death, congestion and oedema of the lungs are regularly developed. 

With disease of the heart, kidneys, and lungs, the congestion, and es- 
pecially the oedema, may be excessive. The lungs may be so completely 
infiltrated with serum as to be unaerated. Such a solid oedema of the 
lungs is sufficient of itself to cause death. It has been asserted by Welch 1 
that the cause of such an excessive oedema is a paralysis of the left side 
of the heart, while the force of the right heart is unimpaired. Such an 
explanation seems to be plausible. 

Patients confined to bed for a considerable length of time may de- 
velop congestion of the dependent portions of the lungs — hypostatic con- 
gestion. The affected portion of lung is shrunken, congested, and im- 
perfectly aerated. 

HEMORRHAGE. 

Extravasations of blood within the air cavities are found with the 
general diseases which produce a disposition to bleeding in different parts 
of the body. 

Blood from the bronchi or from cavities may be inspired into the air 
vesicles. 

Valvular lesions of the heart, especially of the mitral valve, are often 
accompanied by the production of hemorrhagic infarctions in the lungs. 

1 Virchow's Archiv, 72. 



THE RESPIKATORY SYSTEM. 233 

These infarctions are circumscribed, of rounded or wedge-shaped form, 
from the size of a walnut to that of an orange. They are of dark-red 
color, unaerated. the air passages distended with blood, and are often 
surrounded by a zone of pneumonia They may be situated in any part 
of the lungs, but are most common in the lower lobes. When they are 
near the surface of the lungs, a circumscribed pleurisy is often produced. 

Such infarctions may produce death; they may become gangrenous, 
or the blood may become absorbed, or they may be gradually changed 
into a smaller mass of pigmented fibrous tissue. 

It is probable that these infarctions are produced either by thrombo- 
sis of branches of the pulmonary artery, or by rupture of the capillaries. 

Infarctions of smaller size, and with more disposition to be surrounded 
by inflammatory changes, are produced by emboli from the right side of 
the heart, and from thrombi in the veins of pyemic patients. These in- 
farctions are usually situated near the surface of the lung. 

Haemorrhages with rupture of the lung tissue are produced by severe - 
contusions, by penetrating wounds, and by the rupture of aneurisms. 

EMPHYSEMA. 

Emphysema is of two kinds — interlobular and vesicular. 

Interlobular Emphysema is produced by the rupture of air spaces 
and the escape of air into the interstitial tissue of the lung. Or the 
pulmonary pleura may also be ruptured and the air escapes into the 
pleural cavity, or into the mediastinum and from thence into the neck. 
Such a rupture of the air spaces is most frequently caused by broncho- 
pneumonia with consolidation of portions of the lungs. 

Vesicular Emphysema is a dilatation of the air passages and vesicles 
of the lungs. A temporary emphysema can be produced in a variety of 
ways. The bronchi may be obstructed in such a way that the air can 
enter the air spaces, but cannot escape from them. A portion of the 
lungs may be consolidated or compressed, and then the air spaces of the 
rest of the lungs will be dilated. Death may take place with a dilata- 
tion of the lungs, which remains after death. 

Permanent emphysema may change an entire lung if the other lung 
becomes permanently unaerated; it may change portions of a lung if 
other.portions are consolidated. 

" Substantive emphysema " is a term which is now used in a clinical 
rather than in an anatomical sense. It is used to designate a group of 
cases in which there are regularly developed changes in the shape of the 
thorax, certain characteristic physical signs, a liability to bronchitis, to 
constant and spasmodic dyspnoea, to venous congestion of the viscera 
and of the skin. In patients who present such symptoms during life, 
we find after death diffuse changes of both lungs, of which dilatation of 
the air spaces may form a part. If the dilatation of the air spaces does 
17 



234 THE RESPIRATORY SYSTEM. 

exist, the term "substantive emphysema" is appropriate; if it does not 
exist, we employ a term which contradicts itself. 

The real lesion of substantive emphysema is a chronic productive in- 
flammation of the lung with the formation of new connective tissue — a 
process analogous to similar chronic inflammations of the endocardium, 
arteries, and kidneys, and one which, like them, may constitute a for- 
midable disease or an unimportant senile change. 

Both lungs are moderately or considerably increased in size. Very 
often they are partly covered by connective-tissue pleuritic adhesions. 



Pig. 115.— Emphysema, showing Holes in the Walls of the Air Vesicles, x 850 and reduced. 
From a case of chronic miliary tuberculosis. 

The mucous membrane of the bronchi may be coated with mucus or 
with mu co-pus. The muscular coat of the bronchi may be thickened; 
their entire wall may be thickened and infiltrated with cells; they may 
be narrowed or dilated; they may be surrounded by zones of pneumonia. 
The cells which line the walls of the air spaces are increased in size and 
number. The walls of the air spaces are more or less thickened, except 
in the case of some of the air spaces which are dilated. In the walls of 
some of the air spaces, those which are thickened as well as those which 
are thinned, are formed small holes (Fig. 115) which may later reach a 
large size, so that adjacent air spaces become fused together. 



THE RESPIRATORY SYSTEM. 235 

In some cases of substantive emphysema, no dilatation of the air spaces 
exists. In many of the fatal cases, the dilatation is but moderate; in 
some cases it is very marked. The dilatation may involve the air 
passages alone, or both the air passages and the vesicles. It is not uni- 
form, but involves some parts of the lungs more than others. 

The arteries throughout the lungs and in the walls of the larger 
bronchi may have their coats thickened. The capillaries in the walls of 
the air spaces which are but little dilated are unchanged. Those of the 
dilated air spaces are separated by wider intervals; they may be smaller; 
it is said that they may be obliterated. 

The right ventricle of the heart may be dilated or hypertrophied, or 
both. There may be venous congestion of the pia mater, the stomach, 
the small intestine, the liver, the spleen, the kidneys, and the skin. 
There may be dropsy. 

ATELECTASIS. 

A collapsed and unaerated condition of portions of lung tissue is 
either congenital or acquired. 

(1) In congenital atelectasis, portions of the lung are firm, non-crepi- 
tant, of a dark blue or purple color, depressed and smooth on section. 
These portions can usually be artificially inflated, and then cannot be 
distinguished from the surrounding pulmonary tissue. This condition is 
produced by the inability of the child after birth to fully inflate its lungs, 
either from want of sufficient vitality or from obstruction of the bronchi. 
If the child lives for some time, and the collapsed lobules are not in- 
flated, they become hard and dense. 

(2) In youug children, the smaller bronchi may become obstructed 
by the inflammatory products of bronchitis, and the corresponding air 
vesicles will then collapse. We then find scattered through the lungs 
collapsed lobules like those in the new-born child. Inflammatory changes 
may be subsequently developed in the collapsed lobules. 

(3) In adults, large or small portions of lung tissue may become 
collapsed as the result of bronchitis, of stenosis of a large bronchus, of 
compression of a bronchus, of paralysis of the pneumogastric, of com- 
pression of the lungs by fluid or by new growths, and of long-continued 
feebleness of the act of respiration. 

GANGRENE OF THE LtTKGS. 

It is customary to distinguish two forms of gangrene of the lung: the 
circumscribed and the diffuse; yet both can occur together. 

Circumscribed gangrene occurs in the form of one or more rounded 
or irregular masses of variable size. The gangrenous portion of lung is 
at first brown and dry. The surrounding lung tissue is congested or 
cedematous, or infiltrated with blood, or inflamed. If the gangrenous 
focus is near the pleura, the latter will be coated with fibrin. Gradually 



236 THE RESPIRATORY SYSTEM. 

the gangrenous portion of lung assumes a dirty green color and a putrid 
odor. It becomes soft, broken down, and separated from the surround- 
ing lung. The blood-vessels may be obliterated by thrombi, or eroded, 
so that there are profuse haemorrhages. 

Such a gangrenous process may extend to the adjacent lung tissue, 
or a zone of gray or red hepatization or of connective tissue may be 
formed. 

The fluid from the gangrenous lung may pass into the bronchi and 
be expectorated; or it may run from one bronchus into another, and set 
up new gangrenous foci or diffuse gangrene. 

The pulmonary pleura may be perforated, and a gangrenous pleurisy 
produced. 

Diffuse gangrene may follow the circumscribed form; it may com- 
plicate lobar pneumonia, or occur as an idiopathic condition. A large 
part of a lobe or of an entire lung becomes greenish, putrid, and soft, 
and the pulmonary pleura is inflamed. There may be haemorrhages from 
eroded vessels. There may be general septicaemia. 

Various forms of bacteria may be present in gangrenous areas of the 
lungs. Among those frequently present is the Staphylococcus pyogenes 
aureus. 

PNEUMONIA. 

The inflammations of the lung, as distinguished from those of the 
bronchi and pleura, are called '' pneumonia." 

In the present state of our knowledge, the classification of the dif- 
ferent forms of pneumonia must be an arbitrary one. We describe sepa- 
rately: 

Acute lobar pneumonia. 

Broncho-pneumonia. 

Secondary and complicating pneumonia. 

The pneumonia of heart disease. 

Interstitial pneumonia. 

Tubercular pneumonia. 

Syphilitic pneumonia. 

/. Acute Lobar Pneumonia. 

This is an acute exudative inflammation, which involves regularly 
the whole of one lobe, or the larger part of one lung, or portions of both 
lungs. It is an infectious inflammation, attended with the growth in the 
lung of pathogenic bacteria; most frequently the " Diplococcus pneu- 
moniae" of Fraenkel, less frequently the bacillus described by Fried- 
lander. Apparently there are also irregular forms of lobar pneumonia 
attended with the growth of other species of bacteria. 

The inflammation is of pure exudative type, characterized by con- 
gestion, emigration of white blood-cells, diapedesis of red blood-cells, 



THE RESPIRATORY SYSTEM. 23? 

and exudation of blood-plasma, while the tissue of the lung itself is but 
little changed. 

During the first hours of the inflammation, only irregular portions of 
the lobe which is to be inflamed are involved ; later, the entire lobe. 
The lung is congested, oedematous, tough, but not consolidated. The 
air spaces contain granular matter, fibrin, pus-cells, red blood-cells, 
and epithelial cells. The epithelium remaining on the walls of the air 
spaces is swollen ; there are large numbers of white blood-cells in the 
capillaries. The larger bronchi are congested, dry, or coated with 

MWMk 







Fig. 116.— Acute Lobar Pneumonia— Red and Gray Hepatization, x 850 and reduced. 
Showing the pneumococci of Fraenkel in the exudation, stained red. 

mucus ; the small bronchi contain the same inflammatory products as do 
the air spaces. The pulmonary pleura, as a rule, is not coated with 
fibrin. This is called the stage of "congestion." The stage of con- 
gestion regularly. only lasts a few hours, but it may be protracted for 
several days. 

When the exudation of the inflammatory products has reached its 
full development, the presence of these products within the air spaces 
and bronchi causes the lung to be solid, and at this time the lung is 
said to be in the condition of "red hepatization." The lung is now 



238 THE RESPIRATORY SYSTEM. 

consolidated, red, its cut section looks granular, the granules correspond- 
ing to the plugs of inflammatory matter within the air spaces. For some 
time after death the inflammatory products remain solid and the cut 
section of the lung dry; but later, with the commencement of post-mor- 
tem changes, these products soften and the cut section is covered with a 
grumous fluid. The air vesicles, the air passages, the small bronchi, and 
sometimes the large bronchi, are filled and distended with fibrin, pus- 
cells, red blood-cells, and epithelium, and may contain large numbers of 
bacteria (Fig. 116). In spite of the pressure on the walls of the air 
spaces, the blood-vessels in their walls remain pervious. The pulmonary 
pleura is coated with fibrin and the interstitial connective tissue of the 
lung is infiltrated with fibrin. The hepatized lobe is increased in size, 
sometimes so much so as to compress the rest of the lung. About one- 
fourth of the fatal cases die in the stage of red hepatization, at any time 
from twenty-four hours to eleven days after the initial chill. 

After the air spaces have become completely filled with the exudation, 
if the patient continues to live, there follows a period during which the 
exudate becomes first decolorized and then degenerated. This is the 
period of " gray hepatization." The lung remains solid, its color changes, 
first to a mottled red and gray, then to a uniform gray. The coloring- 
matter is discharged from the red blood -cells and the exudate begins to 
degenerate and soften. The lung is found passing from red to gray 
hepatization at any time between the second and the eighteenth day of 
the disease. It is found completely gray at any time from the fourth 
to the twenty-fifth day. About one-half of the cases die in the condi- 
tion of mottled red and gray hepatization ; about one-fourth in the con- 
dition of gray hepatization. 

If the patients recover, the exudate undergoes still further degenera- 
tion and softening and is removed by the lymphatics. This is the stage 
of "resolution." It should commence immediately after defervescence 
and be completed within a few days. But it may not begin until a 
number of days after defervescence, or it may be unusually protracted. 

The pneumococcus of Fraenkel (often also called the Diplococcus 
pneumonias of Fraenkel and Weichselbaum) is the bacterium most often 
present in the lungs in acute lobar pneumonia, and the form which 
there is much reason to believe, in the large proportion of cases, to be 
the cause of the disease. This germ is, in general, round or oval in 
shape, and is apt to occur in pairs or often in longer and shorter chains 
(see Fig. 116). In the tissues, the individual bacteria are frequently 
smaller at one end than at the other, so that they appear lanceolate. They 
are, in the tissues, surrounded by a gelatinous capsule. The Diplococcus 
pneumonias is readily stained by Gram's method. 

It may be artificially cultivated, but its growth is very meagre below 
35°-37° 0., or the temperature of the body. As at this temperature 



THE RESPIRATORY SYSTEM. 239 

gelatin is fluidified, it is usually grown on agar. On this it forms a 
delicate grayish, transparent growth which is very sensitive to the re- 
action of the nutriment, requiring a very slight alkalinity. The growth, 
at best, is not voluminous. It does not apparently grow at all on pota- 
toes. In beef tea it forms a uniform cloudiness and a granular sedi- 
ment. 

A very marked peculiarity of this germ is that it rapidly loses its 
virulence in artificial cultures. Inoculated subcutaneously into rabbits, 
mice, and guinea-pigs, the pure cultures usually induce a fatal septi- 
caemia but no pneumonia. If, however, the virulence of the organism 






:■?. 




Fig. 117.— Acute Lobar Pneumonia with the Production of Organized Tissue in the Air 

Spaces, X 130 and reduced. 
The section shows a number of air vesicles containing organized tissue. 

be reduced by artificial cultivation, the subcutaneous inoculation may 
induce a typical pneumonia, as may also the intrapulmonal injection of 
the virulent cultures. 

An organism identical with the Diplococcus pneumoniae appears not 
infrequently to occur in the mouths of healthy persons. 1 

There is a form of lobar pneumonia in which the inflammation is not 
simply an exudative one, but there is also a growth of new connective 
tissue in the walls of the air spaces and in their cavities (Fig. 117). 

1 For a resume of the studies on the bacterial origin of acute lobar pneumonia, 
consult Baumgarten's tl Mykologie," page 236 et seq. 



210 



THE RESPIRATORY SYSTEM. 



This condition has been usually described as a chronic inflammation 
following an ordinary lobar pneumonia. It seems really to be from the 
outset a special form of pneumonia. For we find, in patients who 
have not been sick for more than a few days, that the pneumonia already 
has its characteristic form. Still further, even in its earlier stages the 
clinical history is somewhat different from that of an ordinary lobar 
pneumonia. 

If the patient dies within three weeks of the commencement of the 
pneumonia, we find one or more lobes consolidated but not much en- 



a? 



w 






^ 



Fig. 118.— Organized Tissue in an Air Vesicle, x 850 and reduced. 



larged. The hepatization is smooth and dense. The walls of the air 
spaces are thickened and coated with an increased number of epithelial 
cells. Some of the air spaces contain only fibrin and pus, but in others 
there is new connective tissue, basement substance and cells (Fig. 118). 
In this new tissue there may be new blood-vessels, which can be -arti- 
ficially injected from the vessels of the lung (Fig. 119). 

If the patient lives for several months, we find the lung very dense 
and smooth. The growth of new connective tissue is more extensive, 
the air spaces are completely filled, their -walls are much thickened, and 



THE RESPIRATORY SYSTEM. 



Ml 



in some places the lung tissue is completely changed into smooth con- 
nective tissue. 




Fig. 119. 



-Air Vesicles containing Organized Tissue in Lobar Pneumonia, x 350 and reduced. 
The blood-vessels are injected with blue. 



II. Broncho-pneumonia (Capillary Bronchitis, Lobular Pneumonia, 
Catarrhal Pneumonia). 

This is the ordinary pneumonia of young children; it is frequent 
also in young persons, but not as common in adults. 

In children, it seems to be due to the same causes which produce 
lobar pneumonia in adults: to the poisons of the different infectious 
diseases; to the inhalation of irritating substances and gases, and of the 
bacteria which produce suppuration. 

In adults, the disease may present itself to us in a variety of ways: 

1. The patients have an ordinary attack of catarrhal bronchitis lasting 
for several days. Instead of getting well promptly, however, the patients 
continue to cough and to feel sick, and, on examining the chest, we find 
a circumscribed area where there is dulness on percussion and loud, 
high-pitched voice. This consolidation of the lung does not, however, 
last very long, and the patients make a good recovery. 

2. The patients are suddenly attacked with a very severe and gen- 
eral broncho-pneumonia. There are chills, a rapid rise of temperature, 

18 



242 THE RESPIRATORY SYSTEM. 

headache, pains in the back and chest, vomiting, great prostration, a 
rapid pulse which soon becomes feeble, very bad breathing — rapid, 
labored, and insufficient — venous congestion of the skin and of the vis- 
cera, cough, at first dry, then with profuse mucus and blood-stained 
sputa, sleeplessness, restlessness and delirium, and albumin in the urine. 
There are coarse subcrepitant and crepitant rales over both lungs, sibi- 
lant and sonorous breathing; the percussion note is normal, or exagge- 
rated, or dull. The disease lasts for from seven to fourteen days, and is 
very apt to prove fatal. 

3. There is a form of broncho-pneumonia in adults which resembles 
lobar pneumonia. There is a general catarrhal bronchitis, with broncho- 
pneumonia and consolidation of one or more lobes. The symptoms and 
physical signs are like those of lobar pneumonia, but with some differ- 
ence. The invasion of the disease is not as sudden, the pulse is more 
rapid, the cerebral symptoms are more constant, the expectoration is 
like that of bronchitis, the physical signs are more slowly developed, the 
duration of the disease is rather longer and resolution is slower. 

4. There is a form of broncho-pneumonia which resembles acute 
phthisis. The patients have a cough with expectoration, at first mucous, 
afterward muco-purulent. There is a moderate fever, with evening exa- 
cerbations and sweating at night. The patients steadily lose flesh and 
strength. The physical signs are those of bronchitis and of consolida- 
tion of parts of the lung. The disease is protracted, continuing as long 
as ten weeks, and is apt to prove fatal. 

With substantive emphysema there may be developed a subacute or 
chronic broncho-pneumonia. 

The essential or constant lesion of broncho-pneumonia is an inflam- 
mation of the walls (not the mucous membrane) of the bronchi, and of the 
air spaces immediately surrounding the inflamed bronchi. The walls of 
the bronchi are thickened and infiltrated by a growth of new cells. The 
walls of the air spaces are thickened, their cavities are filled with fibrin, 
pus, and epithelium, or with new connective tissue. The inflammation 
involves the medium sized and smaller bronchi of both lungs, but is not 
everywhere equally severe; in some parts of the lungs the lesions are 
much more marked than in others. In some of the cases there are no 
other changes, except some general congestion of the lungs. In other 
cases there may be added a catarrhal inflammation of the mucous mem- 
brane of the bronchi, diffuse consolidation of parts of the lung, pleurisy, 
dilatation of the inflamed bronchi, areas of atelectasis, simple or tuber- 
cular inflammation of the bronchial glands. 

The trachea and the larger bronchi are congested and coated with 
mucus. The smaller bronchi contain pus, their walls are thickened and 
infiltrated with cells, and they may be dilated. Around many of the 



THE RESPIRATORY SYSTEM. 



243 



small bronchi are narrow zones of congestion or hepatization. The rest 
of the lungs is congested and cedematons. 

Or the zones of peribronchitic pneumonia are larger, so that a 
section of the lung is mottled with little whitish nodules, each nodule 
corresponding to a cut bronchus surrounded by its zone of pneumonia. 

Or between these zones of peribronchitic pneumonia are areas of 
diffuse hepatization which render portions of the lung completely solid 
(Fig. 120). 





■■2) 



c 






Fig. 120.— Bronchopneumonia in a Child, x 750 and reduced. 
Air vesicles in diffuse hepatization. 

Or there may be areas of atelectasis corresponding to occluded 
bronchi. 

There is often a thin layer of fibrin on the pulmonary pleura. The 
bronchial glands are the seat of simple or tubercular inflammation. 

The dilatation of the bronchi is not constant. When present, it is of 
the cylindrical character and involves the medium-sized bronchi for a 
considerable part of their length. Such dilated bronchi are each of them 



M4 



THE RESPIRATORY SYSTEM. 



surrounded by a narrow zone of pneumonia; the intervening lung tissue 
may be still aerated or hepatized. 

In these peribronchitic zones of pneumonia, the thickening and 
cellular infiltration which exist in the walls of the bronchi extend also to 
the walls of the air spaces. These walls are thickened and infiltrated 
with cells, while the cavities of the vesicles are filled with pus and epi- 
thelium, or with tissue resembling granulation tissue (Fig. 121). In the 
diffuse hepatization, the air vesicles are filled with epithelium, pus, and 
fibrin in varying proportion and quantity; the walls of the air spaces 
remain unchanged. 




Fig. 121. —Broncho-pneumonia in an Adult, x 850 and reduced. 
An air vesicle containing organized tissue in a zone of peribronchitic pneumonia. 



The portions of lung which are not hepatized are congested and 
cedematous. The cavities of the vesicles are diminished by the enlarged 
capillaries, the epithelium is swollen, and in many vesicles a few pus or 
epithelial cells are to be found. 

Such a broncho-pneumonia differs from the ordinary lobar pneumonia 
very decidedly. The inflammatory process is not a superficial one, result- 
ing only in filling the bronchi and air spaces with inflammatory products, 
but it affects also the tissue of the lung, infiltrating the walls of the 
bronchi and of the air spaces. 



THE RESPIRATORY SYSTEM. 245 

This interstitial character of the inflammation seems to be the reason 
why the disease is often protracted and sometimes succeeded by a chronic 
inflammation. This chronic condition we will call " Persistent Broncho- 
pneumonia" 

The original acute broncho-pneumonia is succeeded by a chronic in- 
flammation involving especially the interstitial tissue. 

This inflammation may involve only some of the smaller bronchi and 
small zones of vesicles around them, and then a section of the lung will 
seem to be studded with, fibrous nodules. Or all the bronchi of some 
part of the lung will be inflamed, the peribronchitic zones of pneumonia 






Fig. 122.— Persistent Broncho-pneumonia. 

will become continuous, and so part of a lobe or an entire lobe becomes 
converted into a dense mass of connective tissue. The air vesicles are 
obliterated by the new connective tissue, the interlobular septa and the 
pulmonary pleura are thickened (Fig. 122), and the inflamed bronchi 
may be dilated. The blood-vessels, however, are, for the most part, not 
obliterated, so that the lung does not become necrotic or degenerated, al- 
though occasionally areas of cheesy degeneration exist. 

III % Secondary and Complicating Pneumonia. 

Inflammation of the lungs occurs frequently as a complicating condi- 
tion with lesions of the brain and spinal cord, with pyaemia, with the 



^±6 



THE RESPIRATORY SYSTEM. 



continued fevers, after injuries and surgical operations, and in patients 
who are confined to bed for a long time from any cause. 

The pneumonia developed in these cases may follow one of two dif- 
ferent types. 

1. Part of the lung, usually the posterior portion, is congested, 
leathery, only partly aerated, and mottled by irregular patches of reel 
or gray hepatization which have no relation to the bronchi. In the 
hepatized portions of lung, the air spaces are filled with pus and fibrin. 

2. The inflammation has the characters of a broncho-pneumonia. 
The small bronchi are filled with pus, their epithelium is altered, their 




Fig. 123 —Lobular Pneumonia in a Child, complicating Diphtheria. 
Air vesicle showing inflammatory products and large numbers of bacteria (streptococci J 
stained red with fuchsin. 



walls are infiltrated with pus, and around each bronchus is a zone of air 
vesicles filled with pus and fibrin. The lung is mottled with little whitish 
nodules, corresponding to the bronchi and the peribronchitic zones, 
and between these there may be a diffuse hepatization. 

In children suffering from diphtheria, with pseudo-membranes con- 
taining pathogenic bacteria in the fauces and upper air passages, a sec- 
ondary pneumonia may apparently occur as the result of the entrance 
into the lung spaces of the germs from above (Fig. 123). 



THE RESPIRATORY SYSTEM. 



247 



IV. The Pneumonia of Heart Disease. 

Lesions of the aortic and mitral valves, and dilatation of the left ven- 
tricle, often produce a diffuse, chronic inflammation of both lungs of a 
peculiar character. This condition is often called pigment induration, 
or brown induration, but it is really a chronic pneumonia. 

The lungs are diminished in size, and of a peculiar yellowish-pink 
color, mottled with spots of black or brown pigment. They are not con- 
gested, but are of a dry, leathery consistence; or portions of them may 
be in the condition of a smooth red hepatization. The appearance of 
these lungs may be modified by the presence of hemorrhagic infarctions 
by the pre-existence of emphysema, or by oedema. 





P 








y^ 



--^v 



Fig 124.— The Pneumonia of Heart Disease, x 850 and reduced. 
An air vesicle from a child's lung. 

Minute examination of these lungs shows four separate pathological 
conditions. 

1. A change in the capillaries in the walls of the air spaces. These 
capillaries are dilated and tortuous, so that they project into the cavities 
of the vesicles. The degree of the dilatation varies in the different 
lungs; in some it is very marked, in others but light. 

2. A thickening of the walls of the air spaces, due partly to the dila- 
tation of the capillaries, partly to a growth of smooth muscle, and partly 
to a growth of connective tissue. The degree of the thickening varies 
very much in different cases. 



248 



THE RESPIRATORY SYSTEM. 



3. A formation of black or brown pigment in the shape of granules 
and small masses. This is deposited in the walls of the vesicles, in the 
interstitial connective tissue, and in the new cells within the vesicles. 

4. A formation of cells within the air spaces. The walls of the 
vesicles are 'coated with a layer of flat, nucleated cells. Similar cells, 
or swollen and granular cells, are present in the cavities of the vesicles 
(Fig. 124). If these cells are numerous, the cavities of the vesicles are 
filled, and there results a smooth red hepatization. 

V. Interstitial Pneumonia. 

Moderate degrees of inflammation of the lung, with the production of 
interstitial connective tissue, are common. Such a development of inter- 
stitial pneumouia as to constitute a disease by itself is comparatively rare. 



e 



*-. 







Jr 



%% 








■% 



Fig. 125. 



-Interstitial Pneumonia, x 90 and reduced. 
From a case of chronic phthisis. 



Causes. — Well-marked interstitial pneumonia follows attacks of 
broncho-pneumonia; severe attacks of pleurisy which leave behind ex- 
tensive adhesions; chronic bronchitis; and the inhalation of the dust of 
coal or stone. 

Lesions.— The inflammatory changes are regularly confined to one 
lung, except in the cases of inhalation pneumonia. This lung is thickly 
covered with old adhesions, its pulmonary pleura is thickened; the lung 
itself is small. Bands of dense fibrous tissue extend from the pleura 
into the lung. There is a growth of connective tissue in the septa be- 
tween the lobules, around the bronchi and the blood-vessels, and in the 



THE RESPIRATORY SYSTEM. 



-2U) 



walls of the air spaces (Fig. 125). The cavities of the air spaces are com- 
pressed and obliterated. The mucous membrane of the bronchi is the 
seat of chronic catarrhal inflammation. The walls of the bronchi may 
be thickened and their lumen narrowed; or their walls may be thinned 
with the formation of bronchiectasis. 

The other lung is large and emphysematous. 



A 



-i 



<S' 







^m 







i* 



l^mmm 



Fig. 126. -A Miliary Tubercle, x 300 and reduced. 
Involving only two air vesicles, of which the walls are infiltrated and the cavities filled with 
tubercle tissue. 

Suppurative interstitial pneumonia is sometimes produced in cases of 
septicaemia. The pulmonary pleura is coated with fibrin, the bronchi 
contain pus, portions of the lung are hepatized, and the interlobular 
septa are infiltrated with pus. 

VI. Tubercular Pneumonia. 
The lungs may become the seat of tubercular inflammation as part 
of the lesions of an acute general tuberculosis, or they may be affected 
by localized tubercular inflammations. 
19 



250 



THE RESPIRATORY SYSTEM. 



The localized tubercular inflammations may conveniently be de- 
scribed under the names of : Acute miliary tuberculosis ; Subacute 
miliary tuberculosis; Chronic miliary tuberculosis; Acute phthisis and 
Chronic phthisis. 

Acute Miliary Tuberculosis. — The acute development of miliary 
tubercles in the lungs is usually only part of general tuberculosis, al- 
though the lesion may be most extensive in the lungs. 








wmf 



it 







'*2£T 



',;--H, warn 

fc. 






v*: 






- 



-4 






Fig. 127.— A Miliary Tubercle, X 330 and reduced. 
Formed of several air vesicles filled with tubercle tissue and surrounded by a zone of tissue 
resembling granulation tissue. 



Both lungs are usually involved, but the distribution, number, size, 
and character of the miliary tubercles differ in different cases. 

The larger bronchi are the seat of catarrhal inflammation; the lung 
tissue is congested; the air spaces contain epithelium, pus, and fibrin in 
small quantity. 

The tubercles are found in the parenchyma of the lung, in the con- 
nective tissue forming the septa, along and in the walls of the bronchi 
and blood-vessels, and in the pulmonary pleura. 



THE RESPIRATORY SYSTEM. 



251 



They are scattered singly through the lungs, or aggregated in groups. 
They may be separated by considerable interspaces, or so close together 
that the lung is rendered nearly solid. Some are so small and trans- 
parent that they can hardly be seen with the naked eye; others are 
larger and more opaque. In children's lungs, large masses are found of 
the same structure as miliary tubercles. 

When we examine miliary tubercles as they exist in different lungs, 
it becomes evident that they are not all of the same structure. We find: 

1. Miliary tubercles composed entirely of amorphous granular mat- 
ter, with a few shrunken cells and an external zone of pus cells. These 
cannot be said to have any definite anatomical structure. In some of 



mm 



m 






to 



i $£3k a*. 




>^ 






IS 




w* 



Fig. 128.— A Miliary Tubercle, x 300 and reduced. 
Formed of a number of air vesicles, some containing tubercle tissue, others pus and epithelium. 



them, the outlines of the walls of the air spaces are still visible; in 
others, they are lost in the cheesy mass. 

2. Miliary tubercles composed of a group of air spaces of which the 
walls are infiltrated and the cavities filled (Fig. 126). The walls of the 
air spaces are infiltrated with granulation tissue or tubercle tissue; as 
the infiltration progresses, the blood-vessels are obliterated. Such an 
infiltration may involve symmetrically the whole of the wall of an air 
space, or only a portion of the wall. The cavities of the air spaces are 
filled with tubercle tissue, or with epithelium, fibrin, and pus. 

In some of these tubercles, the tubercle tissue, both in the walls of 
the airspaces and in their cavities, is well developed (Fig. 127); then they 
look like little tumors replacing the lung tissue. In others, the outlines 



252 



THE RESPIRATORY SYSTEM. 



of the walls of the vesicles are preserved, granulation tissue predomi- 
nates, the cavities of the vesicles contain pus, epithelium, fibrin, and less 
tubercle tissue (Fig. 128); then the tubercles look like little areas of a 
composite hepatization. 

In adults such tubercles are small, but in children they may reach a 
large size. 

3. Miliary tubercles, formed by the infiltration of the wall of a bron- 
chiole or air passage with tubercle tissue or granulation tissue. This 
infiltration is apt to involve only one side of the bronchiole or air pas- 






$ 



i^ 












Fia. 129.— Miliary Tubercle in Lung of Child. 
Showingthe Bacillus tuberculosis— stained with fuchsin— ia the contents of the air vesicles and 
in their thickened walls. (.The size of the bacilli relative to other elements is slightly exaggerated.) 



sage. It may be confined to this or it may extend to the walls of the 
adjacent vesicles. These vesicles may remain empty, they may be dilated, 
or they maybe filled with tubercle tissue or with epithelium, fibrin, and 
pus. 

4. Miliary tubercles, formed by the infiltration of the walls of small 
bronchi with tubercle tissue or granulation tissue. The infiltration often 
extends to the surrounding air spaces so as to form tubercles of large size. 

In all these miliary tubercles, there is often cheesy degeneration of 
the central portions. 



THE RESPIRATORY SYSTEM. 



253 



Tubercle bacilli can be demonstrated in most of these miliary tubercles, 
especially in those which have undergone cheesy degeneration (Fig. 129). 

















r^*# 




£&rv 



Fig. 130.— An Aggregation of Miliary Tubercles, x 90 and reduced. 



Subacute Miliary Tuberculosis. — The disease involves only the apex 



If 



Fig. 131.— Diffuse Tubercular Inflammation producing Diffuse Consolidation of the Lung, 

X 300 and reduced. 

of one lung, or one lobe, or portions of both lungs. The inflammation 
may continue for weeks or months, then stop and the patient recover. 
20 



254 



THE RESPIRATORY SYSTEM. 



Or the patient may have a number of attacks, from each one of which he 
recovers. Or the disease may continue, extend, and cause death within 
a few months. Or it may be succeeded by chronic miliary tuberculosis. 
The miliary tubercles are small. Most of them are formed within 
the air spaces or around the bronchioles. They are composed principally 
of tubercle tissue or of round-celled tissue. In the portion of lung 



&b&i 




rW 






vri t 



y^r 





Fig. 132.— An Area of Coagulation Necrosis surrounded by a Zone of Pneumonia, x 40 and 

reduced. 

where the tubercular inflammation is going on, there may also be local- 
ized catarrhal bronchitis and pleurisy. 

Chronic Miliary Tuberculosis. — The morbid process begins at the 
apex of one lung and then slowly extends, either progressively or in at- 
tacks, until a large part of the lungs is involved. 

In the simplest form of the disease, the only change in the lungs is 
the formation of miliary tubercles. These tubercles are harder and 
denser than those found with general tuberculosis or with subacute 






THE RESPIRATORY SYSTEM. 255 

pulmonary tuberculosis. They are composed of tubercle tissue, or round- 
celled tissue, or connective tissue, or are in the condition of cheesy de- 
generation. 

Usually, however, in addition to the miliary tubercles there are other 
changes in the lungs. These additional lesions begin in the same part 
of the lung where the tubercles are formed, and accompany the develop- 
ment of the tubercles in fresh parts of the lungs. 

There may be a localized catarrhal bronchitis. 

There may be an inflammation of the walls of the bronchi, with partial 
destruction of these walls and the formation of cylindrical or sacculated 
bronchiectasis. The walls of the cavities thus formed may be converted 
into connective tissue, or they may remain suppurating and necrotic. 







%>, 



' 




«^. 



Fig. 133.— Tubercle Tissue around an Area op Coagulation Necrosis, x 850 and reduced. 

There may be an interstitial pneumonia with the production of new 
connective tissue, the obliteration of the air spaces, and the consolidation 
of portions of the lungs. 

There may be dilatation of the air spaces of the portions of the lungs 
which are not consolidated (Fig. 130). 

There may be thickening of the pulmonary and costal pleura, with 
connective-tissue adhesions. 

While the morbid process begins as a localized tubercular inflamma- 
tion of the lungs, and often retains throughout this local character, yet 



256 



THE RESPIRATORY SYSTEM. 



it may also happen that from this local lesion other parts of the body 
may be infected. Tubercular laryngitis, and tubercular inflammation 
of the solitary and agminated glands of the small intestine, often com- 
plicate the pulmonary lesion, and sometimes even acute general tuber- 
culosis is produced. 

Acute Pulmonary Phthisis (Acute consumption; Acute catarrhal 
phthisis). — This name is nsed to designate an acute tubercular inflam- 







W 





Fig. 134.— Chronic Phthisis, X 850 and reduced. 
An air vesicle filled with fatty epithelium. 






mation of the lungs combined with other non-tubercular inflammatory 
changes. 

1. In one or more lobes there may be miliary tubercles and a diffuse 
consolidation, due to the filling of the air spaces with fibrin, pus, and 
epithelium. 

2. There is a tubercular broncho-pneumonia involving the smaller 



THE RESPIRATORY SYSTEM. 



257 



bronchi of one or more lobes, and zones of air spaces surrounding these 
bronchi. The walls of the bronchi and of the surrounding air vesicles 
are infiltrated with tubercle tissue. 

3. Besides the tubercular inflammation of the walls of the bronchi 
and of the air spaces surrounding them, there are a general catarrhal 
bronchitis, diffuse consolidation of the lung by the filling of the air 
spaces with fibrin, pus, and epithelium, and fibrin on the pulmonary 
pleura. 

4, Besides the tubercular broncho-pneumonia, the diffuse consolida- 
tion, and the pleurisy, there are small or large portions of dead lung 
tissue in the condition of coagulation necrosis (Fig. 132). These areas 
pass into the condition of cheesy degeneration, and are surrounded by 



ISot 



X' 





WmMmM 



f 



W 



Fig. 135.— Chronic Phthisis, x 850 and reduced. 
Showing growth of connective tissue within an air vesicle. 



zones of tubercle tissue or of round -celled tissue; or they soften and 
form cavities which are in communication with the bronchi. 

5. In addition to the lesions just mentioned, the walls of the bronchi 
are so changed by the tubercular inflammation that cylindrical or saccu- 
lated bronchiectasis are formed. 

Chronic Phthisis. — The lesions are of the same nature as those of 
acute phthisis, but are modified by the long continuance of the inflam- 
mation. 



258 



THE RESPIRATORY SYSTEM. 



1. The air spaces : 

(a) The air spaces are filled with swollen and fatty epithelium (Fig. 
134), or with fibrin and pus, while their walls are unchanged and their 
blood-vessels remain pervious. 

(i) The air spaces are filled and distended with compact fibrin and 
shrivelled pus and epithelium. Their walls are compressed and thin, or 
thickened and infiltrated with cells. The blood-vessels can be only very 
imperfectly injected. This condition may be succeeded by complete 
cheesy degeneration. 

'(c) The walls of the vesicles are thickened, their cavities are filled 
with new connective tissue often containing new vessels (Figs. 135 and 







Fig. 136 —Chronic Phthisis, x 850 and reduced. 
Showing growth of connective tissue within an air vesicle. 

136). This new connective tissue may look like an outgrowth from the 
wall of the vesicle, or as if it was formed free in its cavity. 

(d) There is a diffuse interstitial growth of fibrous tissue and granu- 
lation tissue in the walls of the air spaces, the bronchi and the blood- 
vessels, and in the septa. By this new tissue the air spaces are com- 
pressed and deformed or completely obliterated (Fig. 137). 

2. The nodules: 

These, as in acute phthisis, consist of areas of coagulation necrosis, 
peribronchitic nodules, and miliary tubercles. 

The tubercles may preserve their characteristic structure, or undergo 
cheesy degeneration, or be changed into fibrous tissue (Fig. 138). 






THE RESPIRATORY SYSTEM. 259 

The areas of coagulation necrosis undergo cheesy degeneration, or 
soften and form cavities. They are surrounded by tubercle tissue, or 
granulation tissue, or connective tissue. 

The peribronchitic nodules are much the same as in acute phthisis. 

3. The bronchi: 

The changes in the bronchi in chronic phthisis form a very important 
part of the morbid process. 

(a) The larger bronchi may be the seat of a chronic catarrhal inflam- 




,--" 



Fig. 137.— Interstitial Pneumonia of Chronic Phthisis, x 850 and reduced. 

mation, accompanied by the production of large quantities of mucus and 
pus. 

(b) The bronchi of all sizes may be inflamed, with the production of 
new cells in their walls, in addition to the inflammatory changes of their 
inner surfaces. Such a cellular infiltration of the walls of the bronchi 
is often followed by dilatation — either fusiform or sacculated. 

(c) Tubercle granula and granulation tissue are found in the walls 
of the bronchi. These tissues may degenerate, soften, and thus form 
ulcers. 

(d) The eniire thickness of the wall of a bronchus may become the 
seat of inflammation of a peculiar character. The surface of the mucous 
membrane is coated with pus, the epithelial layer can no longer be seen, 



260 



THE RESPIRATORY SYSTEM. 



the wall of the bronchus is infiltrated with cells. The inflammatory 
products undergo cheesy degeneration, so that we find the inner surface 
of the bronchus coated with cheesy matter, while its wall is also changed 
into cheesy matter. Such a condition of the bronchus is usually followed 
by sacculated dilatation. 

The cavities of chronic phthisis, therefore, are formed by the dilata- 
tion of inflamed bronchi, by the softening of areas of coagulation necro- 
sis, or by the combination of both these processes. 

When cavities are once formed, they are apt to continue and to be- 
come larger as the disease goes on. Their walls may be converted into 
granulation tissue, which ulcerates in some places and proliferates in 








Fig. 138.— An Old Miliary Tubercle converted into Fibrous Tissue, x 90 and. reduced. 

others ; or portions of the wall become necrotic ; or all active processes 
cease and the wall of the cavity is formed of new connective tissue. The 
lung tissue between the cavities becomes compressed and altered in various 
ways. As the cavities increase in size, they touch and open into each 
other. In this way large portions of the lung may be converted into a 
dense mass honeycombed with cavities. 



VII. Syphilitic Pneumonia. 

Persons suffering from inherited or acquired syphilis sometimes 
develop inflammations of the lungs which seem to be due to the sj^philitic 
infection. The lungs may then be affected in several different ways. 



THE RESPIRATORY SYSTEM. 261 

1. There is an interstitial pneumonia beginning around the larger 
bronchi and blood-vessels at the root of the lung, and extending to the 
walls of the air spaces and interstitial connective tissue, so that the 
central portions of one or both lungs are converted into a dense mass of 
connective tissue (Fig. 139). 

2. There is an interstitial pneumonia, with the formation of gummy 
tumors. 

3. There is an inflammation of the wall of the trachea and of the 
larger bronchi. There are ulcers in the mucous membrane, their walls 
are very much thickened, and their cavities are narrowed or dilated. 



1$ 



Fig. 139.— Interstitial Syphilitic Pneumonia, x 170 and reduced. 

4. There are circumscribed areas of interstitial inflammation around 
the smaller bronchi, forming small, hard peribronchitic nodules. 

5. There is a diffuse hepatization, involving lobules or an entire lobe. 
The affected portion of the lung is red or white or grayish. The walls 
of the air vesicles are infiltrated with cells, and their cavities are filled 
with epithelial cells. 

6. There may be a broncho-pneumonia, like the ordinary broncho- 
pneumonia of children ; or a lobar pneumonia, like that of adults. 

7. There may be an obliterating endarteritis of branches of the pul- 



262 



THE RESPIRATORY SYSTEM. 



monary artery, with the formation of white infarctions surrounded by 
zones of connective tissue. 1 

TUMORS. 

Dermoid cysts have been found in the lungs in a few instances. 

Fibromata have been described by Eokitansky. 

Enchondromata may occur both as primary and secondary tumors. 
The primary tumors are small and are believed to originate in the car- 
tilages of the bronchi. The secondary tumors often attain a very large 
size. 



% 



Wm 



%® 



■ ?: \ 






mm < 



® 





m 
w 



Fig. 140.— Primary Carcinoma of the Lung, x 300 and reduced. 

Osteoma is very rare. A case is described by Luschka. 2 

Sarcomata as secondary tumors are of not infrequent occurrence. A 
primary adeno-sarcoma is described by Weichselbaum. 3 

Lymphomata are found in cases of leukaemia and pseudo-leukaemia. 

Carcinoma as a secondary growth may have the form of nodules or 
of diffuse infiltration. Primary carcinoma of the lung has been described 



1 Hiller, Charite Annalen, 1884, p. 184. 

2 Virch. Arch., x., p. 500. 
3 Virch. Arch., 85, p. 559. 



THE RESPIRATORY SYSTEM. 263 

by a number of authors. The new growth (Fig. 140) is in the form of 
small nodules surrounded by pneumonia. As the result of the new 
growth and the pneumonia, a considerable part of both lungs may be 
rendered solid. The bronchial glands are infiltrated, and there may be 
secondary nodules in the pleura. 

The new growth seems to originate in the air spaces. Their walls 
are thickened, their cavities are lined with cylindrical epithelium, or 
filled with cylindrical and polygonal cells, some of which undergo col- 
loid degeneration. 

Or it may originate in the small bronchi. 1 

PARASITES. 

Echinococci occur in the lungs in their ordinary cystic form. The 
sacs may suppurate and discharge through the pleura, the bronchi, the 
wall of the chest, or the diaphragm. 

In bronchiectasis and in gangrenous cavities in the lungs, vegetable 
parasites of various kinds have been described — both moulds and bacteria. 2 

The Bacillus tuberculosis is regularly found in the walls and con- 
tents of cavities in acute and chronic phthisis, sometimes in enormous 
numbers. They are also often present in great numbers in the nodules 
of tubercular inflammation, particularly when these are softening and 
beginning to break down to form cavities (see Tuberculosis). 

THE MEDIASTINUM. 

The anterior mediastinum is situated in front of the pericardium, 
between it and the sternum. At its superior part, the two layers of 
pleurae separate somewhat to inclose the vestiges of the thymus gland; 
behind the second piece of the sternum they are in contact, but below 
this the left pleura recedes from its fellow towards the left side, leav- 
ing an angular space of some breadth. The triangularis sterni muscle 
bounds this space in front. 

The posterior mediastinum, stretching from the pericardium to the 
bodies of the vertebras, incloses between its layers the lower part of the 
windpipe and gullet, the thoracic duct, the descending aorta, the 
azygous vein, the pneumogastric nerve, and some lymphatic glands. 

INFLAMMATION. 

Suppurative inflammation may occur either in the anterior or pos- 
terior mediastinum. It may be caused by fractures, caries, or necrosis 
of the sternum and vertebrae, by perforation of the oesophagus, by sup- 

1 Virch. Arch., Bd. 83, p. 77. 2 Virch. Arch., Bd. 66, p. 330. 



264 THE RESPIRATORY SYSTEM. 

puration of the lymphatic glands, by pleurisy, or may occur without 
discoverable cause. 

The pus may infiltrate the connective tissue, or may form abscesses 
which may attain a large size. The inflammation may extend to the 
pleura or the pericardium; the abscesses may displace the heart, the 
lungs, or the sternum; or they may perforate through the skin into a 
pleural cavity, the oesophagus, the trachea, or a bronchus. 

tumors. 1 

The most common form of new growth in the mediastinum is that 
known by the names of lymphoma, lympho-sarcoma, and lymph-ade- 
noma. 

These tumors are confined to the mediastinum, or they are associated 
with similar growths in other parts of the body in the disease called 
"pseudo-leukaemia." 

Persons between the ages of twenty and thirty years seem to be the 
most liable to the growth, but it is also not uncommon in children. 

The growth begins in the lymphatic glands in the mediastinum, and 
at the root of the lung. It increases at first slowly, then more rapidly, 
and gradually infiltrates the adjoining tissues. In this way, the walls 
of the trachea, bronchi, and aorta, the pericardium, the pleura, and the 
lung, become infiltrated with the growth. The tumor also compresses 
the surrounding organs. 

The growth is composed of a connective-tissue stroma infiltrated with 
small round cells, the relative quantity of cells and stroma varying in 
the different cases. 

Besides this form of tumor, there may also occur in the mediasti- 
num tumors similar to those which grow in the pleura and behind the 
peritoneum, tumors which resemble both the sarcomata and carcino- 
mata and which are difficult to classify. 

Teratoma Myomatodes. — Under this name Virchow describes a very 
remarkable tumor. It grew rapidly in a man, aged twenty-two, of good 
constitution and physical development. The right pleural cavity was 
nearly filled with a solid growth. There were similar growths, of 
smaller size, on the left rib, in the liver, .spleen, and kidneys. The me- 
diastinal tumor consisted of two portions, a larger and a smaller. The 
larger portion consisted of solid tissue, in which were a few cavities. It 
was very vascular. Part of it was composed of dense fibrous tissue. 
The greater portion, however, consisted of loose connective-tissue fibres, 
of fusiform cells, and of large, many-nucleated cells. Some of the fusi- 
form cells were small and of the usual appearance; but many were large, 
and presented striations like those of young voluntary muscle. The 

1 Consult Hare, " Tumors of the Mediastinum," Philadelphia, 1889. 



THE RESPIRATORY SYSTEM. 265 

smaller portion of the tumor looked like a multilobular cystoid. The 
cysts varied much in size, and contained serum, colloid matter, and 
blood. Some of the cysts contained a thick, white material, in which 
were hairs, epidermis scales, ciliated epithelium, and cholestearin. In 
the fibrous tissue about these cysts were pieces of hyaline cartilage. Near 
the surface of the tumor the tissue consisted of a nbro-cellular stroma 
forming alveoli filled with epithelium. The tumor on the third left rib 
consisted of connective-tissue fibres and cells, muscle cells, cysts, alveoli 
filled with epithelium, and a small portion of tissue resembling foetal 
lung. 



THE VASCULAK SYSTEM. 



THE PERICARDIUM. 
INJURIES. 



The pericardium may be wounded by penetrating weapons, by gun- 
shot wounds, and by fragments of bone. It may be ruptured by severe 
contusions of the thorax, and by rapid extravasation of blood into the 
pericardial sac. 

Perforations may be produced by empyema, by mediastinal abscesses, 
by abscesses of the chest wall and of the liver, by aneurisms of the aorta, 
and by suppurative inflammation of the pericardium. 

DROPSY. 

In most post-mortems, we find a little serum, from one-half ounce to 
one ounce, in the pericardial sac. This serum is usually clear and of a 
light yellow color; if decomposition has commenced, it may be of a 
reddish color, or it may be slightly turbid from the falling-off of the 
pericardial epithelium. 

Large accumulations of serum are found as part of general dropsy 
from heart disease, kidney disease, etc. The serum is clear and of a 
light yellow color. Hydro-pericardium is usually moderate in comparison 
with the accumulations of serum in the other serous cavities; sometimes, 
however, there is a very large amount of serum, which hinders the 
movements and interferes with the nourishment of the heart. 

HEMORRHAGE. 

Extravasations of blood in the cavity of the pericardium are pro- 
duced by wounds and rupture of the heart, rupture of the aorta and of 
aneurisms, and occur with pericarditis Small* extravasations in the 
substance of the pericardium are found with scurvy, purpura, fevers, etc. 

PNEUMONATOSIS. 

Air or gas in the pericardium is sometimes found as a post-mortem 
appearance, accompanied with drying of portions of the pericardium. 



THE VASCULAR SYSTEM. 267 

Wounds or paracentesis of the pericardium; the perforation of ulcers 
of the stomach, cavities of the lungs, and ulcers of the oesophagus, may 
admit air into the pericardial cavity. In purulent pericarditis, with 
foul, decomposing exudation, gases may be evolved. 

INFLAMMATION". 

Pericarditis is very rarely a primary lesion. It is most frequently 
associated with rheumatism and Bright^ disease, but is also found with 
pneumonia, pleurisy, phthisis, endocarditis, pyaemia, and may be pro- 
duced by injuries. 

The inflammations of the pericardium resemble those of the pleura. 
They usually begin acutely or subacutely, but may become chronic. 
There is a greater disposition to the escape of blood from the vessels than 
in pleurisy, so that the inflammatory products are often mixed with 
blood. The inflammatory process usually begins at the base of the heart 
and from there extends over the rest of the pericardium. 

Exudative Pericarditis. 

We may distinguish: 

1. Pericarditis ivith the Production of Fibrin. — In the milder exam- 
ples of this form of pericarditis, the pericardium is congested, or also 
studded with minute haemorrhages, its surface is roughened by the depo- 
sition of a thin layer of fibrin. In the more severe cases, the entire sur- 
face of the pericardium is covered with a thick layer of fibrin, and there 
are fibrinous adhesions between the visceral and parietal pericardium. 
If the inflammation continues for any length of time, the pericardium 
itself becomes thickened and infiltrated with cells, and the wall of the 
heart may also undergo inflammatory changes. 

If the patient recovers, the fibrin may be absorbed and the pericar- 
dium return to its normal condition. Or, instead of this, as the fibrin 
disappears there is a growth of new connective tissue which forms per- 
manent thickenings and adhesions of the pericardium, which may after- 
wards become calcified. 

2. Pericarditis tvith the Production of Fibrin and a good deal of 
Serum. — In these cases, the pericardium is coated with fibrin, but, in 
addition, there is a large effusion of serum into the pericardial sac. This 
serum accumulates at first between the floor of the pericardium and the 
lower surface of the heart, and, as it increases, distends the pericardial 
sac in all directions, pushing the heart upward and forward. The 
pericardial sac may be so much distended as to compress the trachea, 
the left bronchus, the oesophagus, or the aorta. If the patients recover, 
the serum is absorbed, and permanent adhesions and thickenings are 
left. 

3. Pericarditis with the Production of Fibrin, Serum, and a good deal 



268 THE VASCULAR SYSTEM. 

of Pus. — This variety may have the purulent character from the outset, 
or it may begin as one of the forms just described, and afterwards assume 
the purulent character. These latter cases are apt to run a chronic 
course. 

In the chronic cases, the pericardial sac contains a large amount of 
purulent serum. The pericardium is coated with fibrin and is itself 
thickened and infiltrated with cells. The walls of the heart may be the 
seat of interstitial myocarditis. In some cases, the products of inflamma- 
tion undergo putrefactive changes; in some cases, the serum is absorbed 
and the fibrin and pus undergo cheesy degeneration; in some cases, ex- 
tensive connective-tissue adhesions and calcific plates are formed. 

4. Tubercular Pericarditis. — This lesion may occur by itself, but is 
apt to be associated with tubercular inflammation in the vicinity of the 
heart. There may be miliary tubercles scattered diffusely, or limited 
to certain regions in the pericardium, which is otherwise little changed. 
Not infrequently, however, there is a considerable thickening of the 
pericardium, either visceral or parietal, or both. 

In such cases, the new-formed tissue consists of fibrous tissue and of 
tubercle tissue which has undergone extensive cheesy degeneration. 
The thickened visceral and parietal pericardium are often more or less 
grown together, so that the pericardial sac may be partially or almost 
completely obliterated. A simple inflammatory exudation of varying 
form often accompanies the tubercular process. 

TUMOES. 

Fibromata sometimes are developed in the pericardium. They are 
often of polypoid form, and from atrophy of the pedicle may become 
free in the pericardial sac. 

Sarcomata and carcinomata occur as secondary growths either from 
continuous infiltration or as metastatic tumors. 

Cysts of the visceral pericardium have been described. 

We have seen a pedunculated cyst containing about six c.c. of clear 
fluid hanging into the pericardial sac from its attachment near the pul- 
monary artery. The origin of these cysts is obscure. 

Endothelioma. — There may be a growth of flat cells arranged in anas- 
tomosing tubules which look like lymphatics, in the pericardium, resem- 
bling similar growths in the pleura. 



THE HEAKT. 
MALFORMATIONS. 

The malformations of the heart are usually closely connected with 
malformations of the aorta and pulmonary artery. They depend on 



THE VASCULAR SYSTEM. 269 

arrest of, or abnormal, development ; on endocarditis, myocarditis, 
thrombosis, or mechanical causes. 

I. The common arterial trunk is only partially, or not at all, separated 
into aorta and pulmonary artery. The divisions between the heart cavi- 
ties are at the same time defective. 

1. There is one ventricle and no auricle. 

2. There is one ventricle and one auricle. 

3. There is one ventricle and two auricles; the aorta is alone or in- 
completely separated from the pulmonary artery. 

II. The trunk of the pulmonary artery or of the aorta is stenosed or 
obliterated, and from the obstruction to the current of blood the develop- 
ment of the septa, between the heart cavities, is prevented. 

1. The aorta, at its origin, or in the ascending portion of the arch, 
is stenosed or closed. The pulmonary artery gives off the descending 
aorta, and supplies the carotids and subclavians. The foramen ovale 
remains open, or there is no septum between the auricles. The ventri- 
cular septum is also usually defective. The right ventricle is hyper- 
trophied. 

2. The pulmonary artery is stenosed or closed. Its branches are sup- 
plied by the aorta, through the ductus arteriosus. The ventricular 
septum is defective, the foramen ovale is open, or the auricular septum 
defective. 

III. The malformation affects the aorta and pulmonary artery after 
they are more fully developed. 

1. There is stenosis of the aorta between the left subclavian and 
ductus arteriosus, or just at the opening of the ductus arteriosus. The 
descending aorta is then a continuation of the pulmonar} 7 ' artery. 

2. The aorta gives off all its branches from the arch, but the 
descending aorta is a continuation of the pulmonary artery; or the 
carotids may spring from the aorta, the subclavians from the pulmonary 
artery. 

3. The vessels are transposed; the pulmonary artery arises from the 
left, the aorta from the right ventricle; the pulmonary veins empty into 
the left, the venae cavaa into the right auricle; or the veins also may be 
transposed. The septa are defective. 

IV. The aorta and pulmonary artery are normal, but the cardiac 
septa are defective. 

1. The foramen ovale remains partly open. This condition may 
continue through life without giving any trouble. 

2. The ductus arteriosus may remain open for many years; this also 
may cause no disturbance. 

3. There is a small or large opening in the ventricular septum. This 
may give rise to no symptoms, unless disease of the heart or lungs be 
superadded. 

21 



270 THE VASCULAR SYSTEM. 

V. Either of the auriculo-ventricular orifices may be entirely closed. 
The foramen ovale remains open, and the ventricular septum is defec- 
tive. 

VI. The valves of the different orifices of the heart may be absent or 
defective. The arteries or the ventricles are usually defective at the 
same time. 

The aortic and pulmonary valves may consist of two large or four 
small leaves, instead of the usual three. The edges of the semilunar 
valves may be fenestrated. These alterations are usually of no signifi- 
cance. 

Generally speaking, the existence of openings between the two auri- 
cles or the two ventricles, admitting some admixture of venous and arte- 
rial blood, produces no marked change in the circulation. If, however, 
the passage of the current of venous blood into the right heart is in any 
way interfered with, the consequences are very serious. Cyanosis is 
produced, the skin is of a bluish color, the small veins and capillaries 
are dilated, exudation of serum and hypertrophy of connective tissue 
take place, especially in the fingers and toes. 

Besides the malformations already mentioned, we may find : 

Entire absence of the heart. 

Abnormal septa and cordse tendineae in the heart cavities. 

Abnormal shapes of the heart. 

Abnormal positions of the heart. 

(a) There is a smaller or larger defect in the walls of the thorax, so 
that the heart projects on the outside of the chest; the pericardium is 
usually absent. 

(b) The diaphragm is absent, and the heart is in the abdominal cavity. 

(c) The heart is in some part of the neck or head; this occurs only 
in foetuses very much malformed. 

(d) The heart is transposed, being on the right side. 

ABNORMAL SIZE OF THE HEART. 

(a) The heart may be abnormally large in connection with obstructive 
anomalies of the great vessels. 

(b) The heart may be abnormally small (hypoplasia). This most 
frequently occurs, according to Virchow, in chlorotic individuals and 
those who are the victims of the hgemorrhagic diathesis. In these cases, 
the aorta and other large arteries are apt to be unusually small and thin- 
walled. 

Very rarely two more or less perfect hearts are found in the same 
thorax. 

CHANGES IN POSITION. 

Changes in the position of the heart are congenital or acquired. The 
congenital malpositions have already been mentioned. 



THE VASCULAR SYSTEM. 271 

The acquired malpositions are caused by: 

1. Hypertrophy of the heart; its long axis approaches the horizontal 
direction. 

2. Changes in the thoracic viscera. Emphysema of both lungs pushes 
the heart downward. Emphysema, pleurisy with effusion, or pneumo- 
thorax of one side pushes the heart to the other side. Pleurisy or chronic 
pneumonia, producing retraction of one side of the thorax, draws the 
heart to that side. New growths, aneurisms, and curvatures of the spine 
displace the heart in various directions. 

3. Changes in the abdomen. Accumulations of fluid and new growths 
in the abdomen, and tympanites, may push the heart upward. 

WOUNDS AND RUPTURES. 

Wounds of the heart are produced by penetrating instruments, by 
bullets, and by fragments of bone. The right ventricle is the more fre- 
quently wounded ; next, the left ; rarely, the auricles. 

The wound may penetrate into the cavities of the heart, or only pass 
partly through its wall, or a bullet or the broken end of a weapon may 
be imbedded in the wall. If the wound penetrates into a cavity, and is 
gaping, death follows instantly, and the pericardium is found filled with 
blood. If the wound be small and oblique, the blood may escape gradually, 
and death may not ensue for several days. In rare cases, adhesions are 
formed with the pericardium, and the wound cicatrizes. "Wounds which 
do not penetrate may cause death by the inflammation which they excite,, 
or may cicatrize. 

Bullets and foreign bodies may become incapsulated in the heart 
wall, and remain so for years. 

Ruptures of the heart wall occur in various ways: 

1. Severe contusions of the thorax may produce rupture, usually of 
one of the auricles. 

2. Spontaneous rupture occurs usually in advanced life. Rupture is 
most frequent in the left ventricle and, in a considerable proportion of 
cases, near the apex. There is usually one rupture, but sometimes 
more. The rupture is usually oblique and larger internally than ex- 
ternally. The heart wall, near the seat of rupture, may be infiltrated 
with blood, or blood may infiltrate the subpericardial fat. The heart 
wall may be of normal thickness, or thin ; it is usually soft and in a con- 
dition of fatty infiltration or degeneration. The rupture very frequently 
takes place when the patient is quiet. Death may be almost instantaneous 
or may not ensue for several hours. 

Fatty degeneration leading to rupture of the heart may be general, 
or it is frequently circumscribed and due to obliterating endarteritis, 
atheroma, thrombosis, or embolus of one of the coronary arteries, whereby 
a portion of the heart wall is deprived of nourishment and degenerates. 



272 THE VASCULAR SYSTEM. 

Or rupture of a branch of one of the coronary arteries may induce rup- 
ture of the heart wall. Acute and chronic myocarditis, with or without 
the formation of abscess or cardiac aneurism, or the presence of tumors 
in the heart wall, or hydatids, may lead to the rupture. 

3. In very rare cases, rupture is produced by stenosis of the aorta 
and dilatation of the heart cavities. 

4. Eupture of the papillary muscles and tendons may be produced by 
fatty degeneration or inflammatory or ulcerative processes. 

ATROPHY. 

Atrophy of the walls of the heart may be accompanied with no change 
in the size of its cavities; or with dilatation (the same as passive dilata- 
tion); or, more frequently, with diminution in the size of the cavities. 

The atrophy involves most frequently all the cavities of the heart, 
but may be confined to one or more of them. 

The muscular tissue appears normal, or brown from the presence of 
little granules of pigment in the muscular fibres, which are sometimes 
present in large numbers; or the muscular fibres may undergo fatty de- 
generation; or there may be an abnormal accumulation of fat beneath 
the pericardium; or there may be a peculiar gelatinous material beneath 
the pericardium: this consists of fat which has undergone mucous degen- 
eration. The heart may be so much atrophied as to weigh four ounces. 

The causes of atrophy of the heart are: 

1. It is a congenital malformation; the heart of an adult then looks 
like that of an infant. 

2. Any chronic and exhausting disease, repeated haemorrhages, old 
age, typhus fever, dysentery, etc., may produce atrophy. 

3. Chronic pericarditis, with large, serous effusion, or with thicken- 
ing of the pericardium, producing constriction of the coronary arteries. 

4. Stenosis, atheroma, calcification, or thrombosis of the coronary 
arteries may produce partial or total atrophy. 

5. Myocarditis, with fatty or fibrous degeneration. 

6. Mitral stenosis may cause atrophy of the left ventricle. 

HYPERTROPHY. 

All the cavities of the heart may have their walls hypertrophied, or 
the thickening may involve one or more. While the wall of a ventricle 
is thickened, its cavity may retain its normal size — simple hypertrophy ; 
or be dilated — eccentric hypertrophy ; or it may be contracted — concen- 
tric hypertrophy. 

Care should always be exercised in judging of this condition, for a 
firmly contracted heart seems to have a small cavity and thick walls. 
The existence of such a condition as concentric hypertrophy is denied 
by some authors. Eccentric hypertrophy is the most common form. 



THE VASCULAR SYSTEM. 273 

Simple hypertrophy is not common, but may occur in connection with 
the atrophied kidneys of chronic diffuse nephritis. The muscle tissue 
in hypertrophied hearts is firmer and denser than normal, and is apt to 
have a darker color. Fatty degeneration may, however, be associated 
with it, giving the walls a lighter appearance. It is probable that the 
increase of tissue in the hypertrophied heart wall is the result of increase 
both in size and number of the muscle fibres. 

Hypertrophy of both ventricles increases both the length and breadth 
of the heart. Hypertrophy of the left ventricle (alone) increases its 
length. The apex is then lower and further to the left than usual. Hy- 
pertrophy of the right ventricle (alone) increases the breadth of the 
heart toward the right side; but sometimes the right edge of the heart 
retains its normal situation, and the apex is displaced to the left. With 
large hypertrophy of both ventricles, the base of the heart may sink, so 
that its long axis approaches a horizontal direction. 

Hypertrophied hearts may weigh from forty to fifty ounces, or even 
more. 

Hypertrophy of the heart may depend upon a variety of causes: 

1. Changes in the valves; either insufficiency or stenosis in the valves 
leading from a cavity, and insufficiency in valves leading to a cavity, may 
induce hypertrophy of its walls. 

2. Obstruction to the passage of blood through the arterial system, 
as in atheroma and other diseases of the intima; congenital or acquired 
stenosis of vessels, pressure of tumors, etc., on vessels; certain forms of 
chronic diffuse nephritis, especially atrophied kidneys, lead to hypertro- 
phy of the left ventricle, and sometimes secondarily to hypertrophy of 
the right ventricle. 

3. Obstruction to the passage of blood through the pulmonary artery 
by stenosis or by certain diseases of the lungs, particularly emphysema 
and chronic phthisis, may lead to hypertrophy of the right ventricle, 
and, secondarily, of the right auricle and left ventricle. 

4. Any cause, whether muscular or nervous, which increases the 
rapidity and force of the heart's contractions, may produce hypertrophy. 

5. Dilatation of the ventricles, from any cause, is frequently followed 
by hypertrophy. 

6. Pericarditis may produce hypertrophy by inducing softening and 
dilatation of the ventricles, or by leaving adhesions which obstruct the 
heart's action. Chronic myocarditis also may lead to hypertrophy. 

Finally, for some cases of hypertrophy no satisfactory cause can be 
found. 

It should be borne in mind that an increase in the amount of fat 
in and about the heart may make the organ appear larger, when there 
may be actually a considerable decrease in the amount of muscle tissue. 



274 THE VASCULAR SYSTEM. 

DILATATION. 

Dilatation may be combined with hypertrophy — active dilatation ; 
or there may be no increase of muscle tissue, but a thinning of the 
walls proportionate to the dilatation of the cavity — passive dilatation. 

Either one or all of the heart cavities may be dilated, the auricles 
most frequently; next the right ventricle; least often the left ventricle. 

Active dilatation has been considered under hypertrophy. 

Passive dilatation may be produced by: 

1. Changes in the valves. Mitral or aortic stenosis or insufficiency 
may produce dilatation of the auricles and right ventricle. Pulmonary 
stenosis or insufficiency may produce dilatation of the right auricle and 
right ventricle. Aortic insufficiency, with or without stenosis or mitral 
insufficiency, may produce dilatation of the left ventricle. Dilatations 
from these causes are often succeeded and compensated for by hypertro- 
phy of the heart's walls. 

2. Changes in the muscular tissue of the heart walls. Serous infil- 
tration from pericarditis, myocarditis, fatty degeneration and infiltra- 
tion, atrophy of the muscle fibres, may all lead to dilatation. 

3. A heart which is already hypertrophied may, from degeneration 
of the muscle, become dilated. 

4. Acute exudative inflammations of the lungs and acute pleuritic 
exudations, by rendering a large number of vessels suddenly imperme- 
able to the blood current, may produce sudden stasis in the pulmonary 
artery and dilatation of the right heart. 

5. There are curious cases of acute and chronic dilatation of the 
ventricles for which no mechanical cause can be found and which are 
very fatal. 

DEGENERATIONS. 

Parenchymatous Degeneration of the Heart Muscle. — This lesion fre- 
quently occurs in typhoid and typhus fever, pyasmia, erysipelas, and 
other infectious diseases, as well as in the exanthemata, as a result of 
burns, and under a variety of other conditions. It is characterized by 
the presence in the muscle fibres of the heart of greater or less numbers 
of albuminous granules of various sizes, most of them very small. They 
are not as refractile as fat-droplets, and are insoluble in ether, while 
swelling up and becoming almost invisible under the influence of acetic 
acid. Sometimes they are so abundant as to conceaL the striations of 
the fibres. The degeneration is usually quite uniformly diffused through 
the heart, whose walls are softer than normal and of a grayish color. 
This lesion may be associated with or followed by fatty degeneration. 

Fatty Degeneration of the Heart Muscle. — This consists in the trans- 
formation of portions of the muscle fibres of the heart into fat, which 
collects in the fibres in larger and smaller droplets, sometimes few in 



THE VASCULAR SYSTEM. 275 

number, sometimes so abundant as to entirely destroy or conceal the nor- 
mal striatums (Fig. 141). These droplets are soluble in ether, and remain 
unchanged on treatment with acetic acid . This degeneration is some- 
times quite universal, but is more apt to occur in patches, giving the 
heart muscle a mottled appearance. This mottling may usually be best 
seen on the papillary muscles. The degenerated areas have a pale-yel- 
lowish color, and the muscle tissue is soft and flabby; but when moderate 
or slight in degree, the gross appearance may be little changed, and the 
microscopical examination be necessary for its determination. This de- 
generation may lead to thinning of the walls, or to rupture of the heart, 
or to inability to fulfil its functions. It is not infrequently the cause 
of sudden death. 

It may be secondary to hypertrophy of the heart, to inflammation of 
the heart muscle, or to pericarditis; to disturbances of the circulation in 
the coronary arteries by inflammation, atheroma, etc. It may be due to 
deteriorated conditions of the blood in wasting diseases, excessive haemor- 
rhages, exhausting fevers, leukaemia, etc., or to poisoning with phos- 



- %V 



Fig. 141. — Fatty Degeneration of the Heart Muscle. Teased. 

phorus and arsenic. It may occur in otherwise apparently healthy 
persons. 

Fatty Degeneration of the Endocardium. — It is not uncommon to 
find, especially in elderly persons, fatty degeneration occurring in 
patches, especially on the valves, but also on the general endocardium. 
They may also occur in ill -nourished and anaemic individuals. Small, 
or even considerable, areas of fatty degeneration appear, as a rule, to be 
of little or no clinical significance. They are at least not inconsistent 
with perfect health. In these areas of fatty degeneration, the connec- 
tive tissue cells are more or less completely filled with larger and smaller 
fat-droplets. 

Amyloid Degeneration of the endocardium or the walls of the blood- 
vessels and intermuscular connective- tissue septa is a not very infrequent, 
but usually not very important lesion. 

Calcification of the products of inflammation in pericarditis, or of 
connective-tissue membranes in chronic pericarditis, sometimes occurs, 
and in the latter case the heart may be more or less inclosed by a calca- 



276 



THE VASCULAR SYSTEM. 



reous shell. The muscle fibres of the heart wall may, though rarely, be- 
come densely infiltrated with salts of lime. 

Fatty Infiltration or Lipomatosis of the Heart. — This lesion, which 
should be clearly distinguished from fatty degeneration, consists of an 
unusual accumulation of fat about the heart and between its muscle 
fibres (Fig. 142). 

The subpericardial fat, which may be present in considerable quantity 
under normal conditions, may be so greatly increased in amount as to 
form a thick envelope inclosing nearly the entire organ. Sometimes 
the accumulation of fat extends into the walls of the heart, between the 
muscles, causing atrophy of the latter, frequently to a very great extent, 
so that the function of the heart is seriously interfered with. This oc- 




Fig. 142.— Fatty Infiltration or Lipomatosis of the Heart. 
The lesion is excessive, the heart muscle being to a large extent atrophied. (The fat-cells are 
represented in the drawing, for the sake of clearness, of relatively too large size.) 



curs sometimes in general obesity, or as a result of chronic pericarditis, 
or in drunkards, or in 'debilitated or old persons. 

Atrophy of the pericardial fat tissue not infrequently occurs in per- 
sons emaciated by chronic disease, and then the usual situations of the 
fat are occupied by a tissue resembling mucous tissue in its gross char- 
acters. Microscopical examination shows that in this atrophic fat the 
fat-cells have largely lost their contents, and the whole tissue has under- 
gone a partial reversion to its original embryonic form (see Fig. 143). 

Myomalacia. — When, through obliterating endarteritis, atheroma, 
thrombosis, or embolus of a branch of the coronary arteries, the blood- 
supply is cut off from a circumscribed portion of the heart wall, the 
tissue in the affected area may undergo fatty degeneration, leading to 



THE VASCULAR SYSTEM. 



277 



rupture. Or, instead of extensive fatty degeneration, the muscle fibres 
may break down into agranular detritus, and the connective tissue about 
them suffer retrograde metamorphosis, so that the whole affected area 
may be soft and yellowish-white or grayish in color. If, as not infre- 
quently occurs, there is considerable extravasation of blood, the degene- 
rated area may be of a dark red color. Under these conditions the wall 
may rupture; or acute inflammatory processes may occur; or the degene- 
rated tissue may be gradually absorbed, and replaced by new connective 
tissue which gradually grows dense, shrinks, and assumes the characters 
of cicatricial tissue. This may occur in any part of the heart wall or in 
the papillary muscles. When the heart wall is involved, the new-formed 




Fig. 143.— Atrophic Pericardial Fat. 
From young person dead of carcinoma of the stomach and peritoneum. Stained with osmic 
acid and teased. 

connective tissue may yield to the blood-pressure from within, and an 
aneurism of the heart be formed. 

INFLAMMATION. 

Endocarditis. 

The endocardium is a connective-tissue membrane which lines the 
cavities of the heart and forms its valves. Its inner surface is covered 
with a layer of endothelial cells. It is but poorly supplied with vessels, 
and the inflammations which attack it are of the cellular variety. The 
ordinary products of inflammation, pus, fibrin, and serum, are scanty, or 
absent altogether. The connective-tissue cells and basement substance 
are principally concerned in the inflammatory processes. The new tissue 
thus produced is prone to degeneration and calcification. The roughen- 
ing of the endocardium due to the inflammation often causes a coagula- 
tion of fibrin on the inflamed surface. 
22 



278 THE VASCULAR SYSTEM. 

In foetal life it is the endocardium of the right heart, in extra-uterine 
life that of the left heart, which is usually inflamed. 

The endocardium which forms the valves is that which is most fre- 
quently inflamed, but the other portions of it are by no means exempt. 

1. Simple Acute Endocarditis. — This is most apt to occur in con- 
nection with rheumatism, but may occur under other conditions. It 
may attack a heart which was previously healthy, or one in which the 
lesions of chronic endocarditis already exist. 

In some cases the only lesion is a simple swelling of the valves. They 
arc thick and succulent, but their surfaces remain smooth. The base- 
ment substance is swollen, and there is a moderate production of new 
connective-tissue cells. 

In other cases, the growth of connective- tissue cells is very much 
more marked, the basement substance is split up, and little cellular, 
fungous masses, called vegetations, project from the free surface of the 



jg) 

I 








Fig. 144.— Vegetation on Aortic Valve in Endocarditis. 
Showing granular thrombus over the surface, 

endocardium. On these roughened surfaces the fibrin of the blood is 
deposited, and so vegetations of considerable size may be formed (see 
Fig. 144). 

In still other cases the cell growth, while in some places it forms 
vegetations, in other places degenerates, and thus portions of the valves 
are destroyed. This is simple acute ulcerative endocarditis. 

In some cases of this disease, the patients recover, and the valves 
seem to return to a normal condition; in other cases the valves are left 
permanently damaged; and in still others chronic endocarditis follows 
the acute form. 



THE VASCULAR SYSTEM. 



279 



2. Mycotic or Malignant Endocarditis (malignant ulcerative endo- 
carditis). 

The direct inciting cause of simple acute endocarditis of the forms 
described above is unknown. But in a considerable number of cases 
of acute endocarditis, bacteria have been found in and about the vegeta- 
tions (see Fig. 145), and proved, by careful experiments, to stand in a 
causative relation to the lesion. 

Those cases of acute endocarditis in which the lesions are induced by 
the direct action of bacteria are called mycotic or malignant or bacteritic 
endocarditis; or, since the new-formed asw T ell as the old tissue about the 
bacteria is apt to become necrotic, and thus lead to larger or smaller 
losses of substance, the lesion is often called ulcerative endocarditis. 

Cultivations of the bacteria occurring in the heart lesions in malignant 
endocarditis have shown that, while various species of bacteria may oc- 




Fig. 145.— Mycotic Endocarditis. 
Section of vegetation showing colonies of micrococci, stained with fuchsin. 

casionally act as an inciting cause, it is most commonly induced by the 
Staphylococcus pyogenes aureus and the Streptococcus pyogenes. 1 

It has been, furthermore, found that a lesion or injury of the endo- 
cardium, either on the heart valves or elsewhere, predisposes to the 
lodgment and growth upon them of the disease-producing bacteria 
when once they have gained access to the circulating blood. 

Mycotic endocarditis is frequently a secondary complicating lesion, 
but may occur as a primary disease. It is most apt to be associated with 
the acute infectious diseases, and in many cases may be regarded as one 
of the local manifestations of pyaemia. 

In some cases, there is a formation of new tissue in the form of 



1 For a detailed consideration of the relationship of bacteria to malignant endo- 
carditis, with experiments and literature, see Prudden, Am. Jour. Med. Sciences 
January, 1887. 



280 THE VASCULAR SYSTEM. 

organized vegetations on the valves or general endocardium; in other 
cases, necrosis either of the Dew-formed or the old tissue is the most 
marked feature. Blood-clots are apt to form on the affected surfaces 
and often largely make up the so-called vegetations. The mitral and aortic 
valves are frequently the seat of the lesion, but it may occur elsewhere. 

Detachment of bacteria containing fragments of the vegetations or 
clots may give rise to single or multiple infectious emboli (see p. 58) 
and abscesses in various parts of the body, such as spleen, kidneys, 
brain, skin, heart wall, etc. Bacteria similar to those in the heart lesion 
may be found in these secondary abscesses (see Fig. 31). 

It is probable that these abscesses in ulcerative endocarditis do not 
always arise from cardiac emboli, but may precede the heart lesion. 

3. Chronic Endocarditis may succeed acute endocarditis, or the in- 
flammation may be chronic from the outset. It affects most frequently 
the aortic and mitral valves, and the endocardium of the left auricle and 
ventricle; similar changes in the right side of the heart being much less 
frequent. 

There are two main anatomical varieties of chronic endocarditis, 
which may occur separately or together. 

(1) The endocardium is thick and dense, its surfaces are smooth or 
covered with small, hard vegetations or ridges; it is often infiltrated with 
the salts of lime. 

(2) There is a growth of connective-tissue cells in the endocardium, 
with a splitting-up of the basement substance. Some of the new cells 
continue to live, others degenerate. By the combination of such a cell 
growth and destruction, the endocardium is in some places destroyed, in 
others changed into projecting vegetations. Fibrin is deposited on the 
roughened surfaces. After a time, the condition may be further com- 
plicated by the shrinkage and deposition of the salts of lime in the new 
tissue and in the endocardium. All these changes may extend to the 
wall of the heart beneath the endocardium. 

The most important result of chronic endocarditis is its effect on the 
heart valves, producing insufficiency and stenosis. The changes in the 
valves are followed by changes in the walls and cavities of the heart, 
and disturbances of the circulation throughout the body. 

4. Chronic Ulcerative Endocarditis. — Large ulcers or perforations of 
the valves may be formed in chronic endocarditis, upon which clots may 
form, so that in gross appearance a great similarity exists between this 
and malignant ulcerative endocarditis, particularly if the latter have 
been ingrafted upon an already chronically diseased endocardium. The 
microscopical and biological examinations must usually be resorted to in 
order to determine the exact significance of the lesion. 

5. Tubercular Endocarditis may occur in connection with tuber- 
cular pericarditis or general miliary tuberculosis. The tubercles may be 



THE VASCULAR SYSTEM. 281 

small and single, or grouped in masses, and show the usual degenerative 
changes. 

Myocarditis. 

The inflammatory changes in the walls of the heart involve primarily 
the interstitial tissue and blood-vessels, the muscle fibres being seconda- 
rily affected by atrophic and degenerative changes. 

There is a change in the muscle fibres by which they are broken into 
rectangular fragments, with a collection of granular matter around the 
nuclei, the entire tissue becoming dense and translucent. This change 
is sometimes called ""parenchymatous myocarditis/' but its inflammatory 
nature is doubtful. 

Interstitial Myocarditis may be acute and purulent, or chronic with 
the formation of new connective tissue. 

Acute Purulent Myocarditis may be diffuse, infiltrating the wall of 




Fig. 146.— Chronic Interstitial Myocarditis. 
Showing transverse section of a portion of a papillary muscle. 

the heart with pus. This may occur as a complication of scarlatina and 
from unknown causes. 

More frequently the purulent inflammation is circumscribed, produc- 
ing abscesses. These occur with pyaemia, mycotic ulcerative endocardi- 
tis, and other infectious diseases. They are of different sizes, and either 
single or multiple. They are produced by the lodgment of infectious 
emboli in small vessels. The contents of the abscesses consist of pus, 
broken-down muscle tissue, and bacteria. These abscesses may open 
into the pericardial sac and set up a purulent pericarditis; or into a 
heart cavity, giving rise to thrombi in the heart and emboli in different 
parts of the body; or the wall of the heart is weakened by the abscess, 
so that it ruptures, or an aneurismal sac is formed; or an abscess in the 
interventricular septum may establish an opening bet ween the ventricles; 
or the suppurative process may extend upward and form an abscess in 
the connective tissue at the base of the heart. 
23 



282 THE VASCULAR SYSTEM. 

In rare cases, the patients recover, the contents of the abscesses be- 
come dry and hard, and inclosed by a wall of fibrous tissue. 

Chronic Interstitial Myocarditis may be secondary to pericarditis or 
endocarditis, to obliterating endarteritis of the branches of the coronary 
artery, myomalacia, or may occur by itself. There is a growth of new 
connective tissue or of granulation tissue between the muscular fibres, 
with atrophy and degeneration of the muscle. This growth may be in 
the form of circumscribed patches (Fig, 146), or diffused over a con- 
siderable part of the wall of the heart. Such an interstitial inflammation 
is often followed by dilatation of the cavities of the heart, by the forma- 
tion of aneurisms of the wall of the heart, and of thrombi in the cavities 
of the heart. 

Syphilitic Myocarditis is accompanied by the growth of connective 
tissue or granulation tissue in the wall of the heart between the muscu- 
lar fibres. The pericardium and endocardium may also be thickened, 
and pericardial adhesions may be formed. Gummata of the heart are 
of rare occurrence. 

CHANGES IN THE VALVES. 

Fenestration of the valves is usually a change productive of no bad 
consequences. It occurs very frequently in the aortic and pulmonary 
valves. The valves may be thinner than usual, and close to their free 
edges are small slits extending from the centre to the attached edges of 
a leaf. 

Aneurisms of the valves are produced in two ways: 

1. They are the result of endocarditis. One of the lamellae of the 
leaf of a valve is destroyed, and the other lamella is converted into a sac 
filled with blood. These aneurisms are found in the aortic valve, pro- 
jecting into the ventricle; and in the mitral valve, projecting into the 
auricle. Not infrequently the wall of the aneurism gives way, so that 
there is a rupture entirely through the valve. 

2. The entire thickness of a leaf of a valve is converted into a sac 
filled with blood. This occurs in the aortic, mitral, and tricuspid 
valves; its cause is unknown. 

Haemorrhage in the substance of the valves is sometimes found in 
very young children. It does not appear to have much clinical impor- 
tance. 

ANEUEISM OF THE HEAET. 

Sacs filled with blood, situated in the walls of the heart and com- 
municating with its cavities, are formed in several different ways. 

1. In consequence of inflammatory processes in the endocardium 
and muscular tissue, a small or large portion of the wall is converted into 
fibrous tissue. The portion thus changed no longer resists the pressure 



THE VASCULAR SYSTEM. 283 

of the blood from within, and is driven outward. Such a pouch may 
be a circumscribed sac, communicating with the heart cavity by a 
small opening, or may look like a dilatation of part of the ventricle. 
The wall of such an aneurism becomes thinner as the sac increases in 
size. It is composed of the endocardium, new fibrous tissue, visceral 
pericardium, and sometimes the adherent parietal pericardium. The 
walls may calcify, or rarely they become so thin as to rupture externally 
or into the right ventricle. The sacs may contain fluid blood or be filled 
up with fibrin. 

Such aneurisms are usually situated in the wall of the left ventricle; 
rarely in that of the left auricle. If they are in the septum, they may 
project into the right ventricle. They are usually single, but sometimes 
two or three are found in the same heart. 

2. Fatty degeneration of the heart wall may reach such a point that 
the wall yields and is pouched out into an aneurismal sac. 

3. Endocarditis and myocarditis, or fatty degeneration, may so 
soften a portion of the heart wall that the endocardium and part of the 
muscular tissue are ruptured, and a ragged cavity is formed. This form 
of aneurism usually does not attain a large size, but soon ruptures exter- 
nally, and causes the death of the patient. 

THROMBOSIS OF THE HEART. 

It is very common to find after death, in the heart cavities, yellow, 
succulent, semi-translucent masses. They are most common and of firm- 
est texture in persons who die of acute inflammatory diseases. They 
may adhere quite firmly to the walls of the heart, and may extend in 
long, branching cords into the vessels. They are formed in the last 
hours of life and just after death. They have no clinical or pathologi- 
cal importance. 

Coagulations of the fibrin of the blood in the heart do, however, occur 
during life, and -may exist for years. If the fibrin adheres to the valves 
in small masses, these are called vegetations; if it coagulates in the heart 
cavities in larger bodies, they are called thrombi or heart polypi. 

Such thrombi are found in all the heart cavities. They form flattened 
masses firmly adherent to the endocardium; or rounded bodies in the 
spaces between the trabecule; or have a polypoid shape and are attached 
by a narrow pedicle, or are free in the cavity. 

They are usually found in connection with some valvular lesion 
which prevents the free circulation of blood through the heart. 

They are firm, dry, and of a whitish color; they may soften and 
break down at their centres, so as to look like cysts filled with pus, or 
they may calcify. They are usually entirely unorganized, consisting 
simply of fibrin. 



284 THE VASCULAR SYSTEM. 

One of us (Delafield) has seen an organized thrombus in the heart of 
a man, whose history was unknown, who was found dead in the street. 

Sometimes sarcomatous and carcinomatous tumors in different parts 
of the body are accompanied by the formation of thrombi in the heart 
cavities which are composed partly of coagulated blood, partly of tis- 
sue like that of the primary tumor. 

TUMORS. 

Primary tumors in the heart are rare; but sarcomata, myxomata, 
fibromata, and lipomata may occur. Rhabdomyomata, probably con- 
genital, may occur in the heart wall as circumscribed nodular masses. 
A cavernous tumor of this kind has been described. Secondary tumors, 
as a result of metastasis, or of continuous growth from adjacent parts, 
are not very infrequent. These are usually carcinomata or sarcomata. 
Secondary chondromata have been observed. 

PARASITES. 

Echinococcus sometimes occurs in the heart wall and may perforate 
into the cavities. Cysticercus cellulosae has been observed. 

THE BLOOD-VESSELS. 
ATROPHY AND HYPERTROPHY. 

Atrophy of the blood-vessels may involve the entire trunk or some of 
its elements. It may occur as a part of general malnutrition of the 
hody, or in connection with atrophy of particular organs, or as an ac- 
companiment of various diseases of the vessels themselves. 

Hypertrophy, which is especially seen in the arteries, may occur in 
the establishment of a collateral circulation upon the closure of arterial 
trunks, or it may occur as the result of increased blood-pressure, as in 
some forms of hypertrophy of the heart. 

DEGENERATION". 

Fatty Degeneration. — This may occur in the walls of otherwise unal- 
tered vessels, or in those which have undergone a variety of inflamma- 
tory or degenerative changes. It may occur either in the intima or 
media, or both, and may be so extensive as to form a very prominent 
gross lesion, or so little developed as to require the microscope for its 
recognition. When marked, especially if occurring in the intima of large 
vessels, smaller and larger spots or stripes or patches may be seen, of a 
yellowish-white color, usually sharply circumscribed, and sometimes 
smooth, sometimes roughened on the surface. It is most apt to occur in 
the aorta, but may be found in any of the vessels. In moderate degrees 



THE VASCULAR SYSTEM. 285 

of the lesion, we find on section that the cells of the intima contain fat- 
droplets in greater or less number. When further advanced, not only 
are the cells crowded with fat-droplets, but the intercellular tissue also 
may be more or less densely infiltrated with them. Sometimes the in- 
filtration is so dense that the tissue breaks down, and there may be an 
erosion of the surface, forming a so-called fatty ulcer. When the media 
is involved, the muscle cells contain fat-droplets. It may lead to the 
formation of aneurism or to rupture of the vessels. 

Calcification usually occurs in vessels otherwise diseased, and may in- 
volve either the intima or media. It consists in the deposition of salts 
of lime either in the cells or intercellular substance. The lime may be 
in the form of larger or smaller granules or in dense translucent plates. 

Amyloid Degeneration, which may affect all the coats of the arteries, 
but especially the intima and media, will be considered under the lesions 
of the organs in which it most commonly occurs. 

Hyaline Degeneration may cause thickening of the intima of the 
blood-vessels by its conversion into or infiltration with a homogeneous 
material somewhat similar to amyloid (see page 68). Or it may involve 
the entire wall of smaller vessels, converting them into irregular lumpy 
cords . The lumen of vessels thus changed may be obliterated or occluded 
by thrombi. 

THE ARTERIES. 
INFLAMMATION. 

Acute Arteritis. 

Acute inflammation of the walls of the arteries is, in the majority 
of cases, the result of injury, or of an inflammation in the vicinity of the 
vessel, or of the lodgment within it of some foreign body of an irritat- 
ing or infectious nature. The inflammatory process may be largely con- 
fined to the inner layer of the vessels— endarteritis; or it may com- 
mence in the outer layers— periarteritis; or it may involve the entire 
wall. 

The blood-vessels in the outer layers may be congested, the tissue 
oeclematous and infiltrated with pus cells, and the entire wall may be- 
come necrotic. The intima, if this layer is involved, loses its natural 
gloss, looks dull and swollen. It may become infiltrated with pus from 
the outer layers, and it may become necrotic. Under these conditions 
thrombi usually form, and in these may occur the various changes which 
have been already described on page 56. 

Chronic Arteritis. 

In chronic arteritis, all the coats of the vessel may be involved, but in 
most cases the lesion is either largely confined to, or most marked in, the 



286 



THE VASCULAR SYSTEM. 



intima — endarteritis. The disease may supervene upon an acute inflam- 
mation of the artery, or it may be chronic from the beginning. The 
inflammation may occur in patches or in irregular segments of the ves- 




•y-wv 



Fig. 147.— Chronic Endarteritis. 



Involves one of the cerebral arteries. The amount of thickening of the intima is in this case 
moderate. 

sels, of various lengths, or it may occur diffusely. It may be limited to 
single arterial trunks, or it may affect more or less all the arteries of the 
body. Arteries which are the seat of slight degrees of chronic inflam- 
mation may appear to the naked eye but slightly, or even not at all, 





•y-K?/M : -i-- • T4» .V 1 .' •»•'#*' 









Fig. 148.— Chronic Obliterating Endarteritis. 
The lesion in this case is excessive, almost entirely closing the lumen of the vessel. There is, 
too, a moderate degree of periarteritis. 

changed, or the walls may seem stiffer than usual, and remain widely 
open when cut across. When the lesion is more marked, whitish patches 
or areas of distinct thickening of the wall may be seen, which sometimes 



THE VASCULAR SYSTEM. 



287 



visibly incroach upon the lumen of the vessel (Fig. 147). Microscopical 
examination shows that the thickening of the wall is due to the forma- 
tion of new connective tissue, mostly in the intima. The new tissue 
may be soft and gelatinous in character and contain few or many cells; 
or it may be very dense and hard and contain very few cells. The 
endothelial layer of the intima may remain intact over the thickened 
area. Parts of the vessel not distinctly thickened may contain an 
unusual number of small spheroidal cells. Sometimes the musculosa 
and adventitia as well as the intima show at the seat of thickening an 
increase of new connective tissue. The increase of connective tissue in the 
intima, particularly of smaller arteries, may be so great as to incroach 
seriously upon the lumina, and even lead to their obliteration — endar- 
teritis obliterans (Fig. 148). Obliterating endarteritis is very common 
in the interstitial inflammation of organs, such as the kidney, liver, etc., 




Fig. 149.— Atheroma of the Aorta, with Degeneration of New-formed Tissue. 
a, adventitia; b, media; c, new tissue developed in the intima; d, degenerated area; e, area of 
softening; g, fat-droplets in softened area. 

as a part of the general new formation of connective tissue. Arteries 
which are the seat of chronic arteritis are not infrequently the seat of 
secondary acute inflammatory changes, so that, in addition to the forma- 
tion of connective tissue, they may become infiltrated with small 
spheroidal cells, which may lie singly or in clusters in the various layers, 
and particularly along the blood-vessels of the adventitia. 

Arteries which are the seat of chronic endarteritis are liable to suffer 
a series of degenerative changes, consisting chiefly of fatty degeneration, 
calcification, or the breaking-down of the degenerated tissue, and the 
formation of inclosed softened areas (Fig. 149), or erosions or ulcer-like 
openings in the intima. To the varied alterations produced in the walls 
of the arteries by combinations of these inflammatory and degenerative 
changes the name atheroma is frequently applied. 

When fatty degeneration supervenes upon chronic endarteritis, the 



288 THE VASCULAR .SYSTEM. 

thickened areas may have a light-yellowish color, and the microscopical 
examination will show a greater or less amount of fat in and between the 
cells of the intima or the new tissue produced therein. Should the 
fatty degeneration be extensive, the basement substance and the cells 
may gradually disintegrate, and larger and. smaller irregular cavities 
may be formed in the walls, filled with fat-droplets and tissue detritus. 
These softened areas, sometimes called atheromatous cysts, frequently 
also contain cholestearin, and there may be partial calcification of their 
contents, or of the tissue of the arterial wall about them. Sometimes 
the wall of the artery, instead of undergoing simple fatty degeneration, 
or in connection with this change, becomes in circumscribed localities 
looser in texture by the conversion of the muscular and connective 
tissue into a finely fibrillar substance which may persist for some time or 
break down, forming an atheromatous cyst. These atheromatous cysts 
may, through a degeneration of the tissue inclosing them, open into the 
lumen of the vessel, forming the so-called atheromatous ulcers. Frag- 
ments of tissue from the edges of these ulcers, or from the contents of 
the cysts, may be carried into the circulation, forming emboli. Fibrin- 
ous thrombi are prone to form upon the roughened surface of the 
intima or upon the surface of the erosions. Very frequently the calci- 
fication is so extensive that large, hard, calcareous plates are formed in 
the walls and may project inward, forming roughened surfaces on which 
thrombi are deposited. Fatty degeneration and calcification of the 
media and thickening of the adventitia may occur in connection with 
atheroma of the intima. Sometimes the vessels by these changes 
become greatly deformed, so that over considerable areas the entire wall 
may be altered, presenting raised and roughened surfaces interspersed 
with calcareous plates, erosions, thrombi, etc. Chronic endarteritis 
and atheroma is most common and marked in the aorta, but it may 
occur in smaller arteries, particularly in the cerebral and coronary 
arteries. 

Arteritis as a result of syphilis is of frequent occurrence. This may 
lead to partial or complete obliteration of the lumen of the vessel by 
a thickening of the intima (Fig. 95), or it may involve all the arterial 
coats. Histologically the new tissue formed in syphilitic arteritis is 
identical in most cases with the product of simple chronic inflammation; 
but when arteries are involved in the growth of gummy tumors, the 
cheesy degeneration characteristic of the latter often affects the vessels 
also. Syphilitic arteritis is apt to affect smaller vessels, and the degene- 
rative changes do not form so prominent a feature as in other forms. 

In tubercular inflammation, the walls of the arteries, particularly the 
smaller ones, may be thickened, and their lumina obliterated (Fig. 150). 

The results of arteritis vary greatly, depending upon the size and 
situation of the affected vessel, and the extent and particular form which 



THE VASCULAR SYSTEM. 



289 



the lesion assumes. The vessels may become dilated by a yielding to the 
blood-pressure of their weakened walls, aud aneurisms of various kinds 
may be thus produced. Thrombi and emboli may be induced by means 
of the roughened surfaces common in endarteritis, particularly of the 
larger vessels. On the other hand, obliterating endarteritis may cause a 
partial or entire shutting-off of the blood-supply to a part, and a more or 
less serious interference with its nutrition, or even its death. Hyper- 
trophy of the left ventricle of the heart may accompany extensive 
arteritis, as a result of the increased rigidity of the walls of the vessels, 
or the diminution of their lumina. 














Fig. 150. — Tubercular Arteritis in the Lung. 



Showing the iucroachment of an area of tubercular inflammation upon the wall of the artery 
and the formation of a mass partly occluding the lumen of the vessel. This section shows how- 
the generalization of the tubercular inflammation through the body may occur by the sweeping 
away of the tubercle bacilli by the blood and the establishment of new foci in various parts of the 
body. From specimen prepared by Dr. J. S. Ely. 

It is important to remember that a very slight contraction of arteries 
which have undergone a considerable degree of obliterating endarteritis 
may produce, for the time being, the same effect upon the part supplied 
by them with blood that a permanent occlusion would do. Such an oc- 
clusion of the vessels and cutting-off of the blood-supply may be of the 
greatest significance, even though it be but temporary, if it involve 
branches of the coronary or cerebral arteries. Although it is not yet 



290 THE VASCULAR SYSTEM. 

proven that temporary contraction of partially occluded arteries is a 
sufficient or frequent cause of sudden death, there are cases of sudden 
death with the symptoms of heart failure or with the symptoms of hemi- 
plegia, in which the only discoverable lesions are obliterating endarteritis, 
respectively, of the coronary or cerebral arteries. We have seen cases of 
sudden death occurring with symptoms of hemiplegia, in which there 
was, at some point of the middle cerebral artery, considerable, although 
not complete, obliteration of the vessel, but no evidence of degeneration 
of the brain tissue supplied by it. 1 

The causes of chronic arteritis and atheroma are in many cases not 
understood. It may commence in an acute process, or it may be slow in 
its development. It is very common in old people, and seems often to 
be of no particular significance. On the other hand, it may, as we have 
seen, particularly in the smaller arteries, be associated with syphilis, tu- 
berculosis, or interstitial inflammation of organs. 

DILATATION AND ANEURISM. 

1. Cirsoid aneurism consists in the dilatation and lengthening of 
large or small arteries. The walls of the artery are thinned, the vessel 
is tortuous and in places sacculated. These changes are most frequent 
in small arteries, especially the temporal and occipital; they involve the 
trunk of the vessel and its branches, or may extend to the capillaries and 
small veins. They form larger or smaller tumors beneath the skin. 

Karely they are found in the larger arteries, and even in the aorta. 

2. The ordinary aneurism is a dilatation of the coats of the artery 
over a larger or smaller part of its course. Such dilatations are usually 
due to chronic endarteritis and atheroma. According to their shape, we 
may distinguish two varieties : the diffuse and the circumscribed. 

(a) The diffuse, cylindrical, or fusiform aneurism consists in a uni- 
form dilatation of all the coats of an artery, so that it assumes the shape 
of a fusiform or cylindrical swelling. In the walls of the dilated portion 
of the vessel there are often smaller, circumscribed dilatations. The 
wall of the aneurism is atheromatous or calcified; the middle coat may 
be atrophied. The arch of the aorta is the most common seat of this 
form of aneurism, but the entire length of the aorta, or parts of any 
other arteries, may be dilated in the same way. 

(b) The circumscribed or sacculated aneurism consists either in a 
dilatation of the entire circumference of an artery over a short portion 
of its length, or in a dilatation of only a small portion of one side of the 

'Consult CohnJieim and v. ScJuilthess-Bechberg, "Ueber die Folgen d. Kranz- 
arterienverscbliessung fur das Herz,'' Virch. Archiv, Bd. 85, p. 503; also Leyden, 
■' Ueber d. Sclerose der Coronar-Arterien u. d. davon abbangigen Krankbeitszu- 
stande," Zeitscb. f. klin. Med., Bd. vii., pp. 459 and 539. 



THE VASCULAR SYSTEM. 291 

wall, so that the aneurism looks like a swelling attached to one side of 
the artery. The aneurism commences as a dilatation of all the coats of 
the vessel; but as soon as it attains any considerable size, the middle 
coat atrophies, so that the wall is composed of the inner and outer coats; 
or the inner coat is destroyed by endarteritis, so that the outer coat alone 
forms the wall of the aneurism. As the aneurism increases in size, it 
presses upon and causes the destruction of the neighboring tissues and 
viscera, and portions of these tissues and viscera become incorporated 
with or take the place of the wall of the aneurism. The cavity of the 
aneurism is filled with fluid or clotted blood, or with layers of fibrin 
which adhere closely to its wall. The communication between the aneu- 
rism and the artery may be small or large. If arterial branches are given 
off from the aneurism, they may remain open or become plugged with 
fibrin; or their walls are thickened and their cavities narrowed by endar- 
teritis. JDeath is produced by the pressure and interference of the aneu- 
rism with the adjoining viscera, or by rupture. The rupture may allow 
enough blood to escape to destroy life, or the blood may be held in by 
the soft parts, and a second false aneurism formed about the original one. 
Dissecting aneurisms are those in which, owing to a solution of con- 
tinuity of the inner layers of the artery, the blood gets between the 
media and adventitia, and forces its way for a greater or less distance 
between them. Or it may separate the media into two layers. 

ANEURISMS OF THE DIFFERENT ARTERIES. 

The aorta may be dilated over its entire length; or there may be dif- 
fuse or circumscribed dilatations at any portion of its course; or there 
may be several aneurisms, situated at different points. The ascending 
portion of the arch of the aorta may be uniformly dilated in a fusiform 
shape; or there may be circumscribed dilatations on its anterior wall, or, 
more rarely, on its posterior wall. The sacculated aneurisms may be of 
all sizes, and may rupture within the pericardium; or they may form a 
-cavity in the upper part of the ventricular septum, and communicate by 
openings into the pulmonary artery and left ventricle; or they may dilate 
downward between the visceral and parietal pericardium, in front of the 
heart, pushing that organ backward. They may perforate into the right 
•or left auricle or right ventricle, the superior vena cava, or the pulmo- 
nary artery; or they may reach a large size, press on and erode the right 
side of the sternum and adjoining ribs, project under the skin, and even 
rupture externally. 

The transverse portion of the arch may be dilated in a fusiform 
shape; or there may be sacculated aneurisms at any point in its wall. 
The sacculated aneurisms usually reach a considerable size. They press 
on the sternum and ribs in front, or on the oesophagus, trachea, and 
bronchi behind. The large arteries given oif from the arch may be oc- 



292 THE VASCULAR SYSTEM. 

eluded. They cause death by pressure ou the air passages, the oesopha- 
gus, and the vena cava; or may rupture externally or into the oesopha- 
gus, trachea, bronchi, or pleural cavities. 

On the abdominal aorta we usually find aneurisms sacculated. If 
they are situated high up, they may project into the pleural cavities; if 
lower down, into the abdomen. They may compress and displace the 
viscera, vessels, and nerVes, and erode the vertebrae. They may rupture 
behind the peritoneum, into the peritoneal cavity, the pleural cavities, 
the inferior vena cava, the lungs, the colon, the pelves of the kidney, 
or the posterior mediastinum. 

The coronary arteries may be dilated throughout, or may be the seat 
of small sacculated aneurisms. These may rupture into the pericar- 
dium, or may cause rupture of the heart wall. 

The pulmonary arteries are rarely the seat of aneurisms. Diffuse 
and circumscribed dilatations, however, sometimes occur on the main 
trunk and on the two principal branches of the artery. They do not 
usually reach a large size, but may cause death by rupture. General 
dilatation of all the branches of the pulmonary artery is more common. 
It is found in connection with stenosis of the mitral valves, and with 
compression or induration of the lung tissue. 

Of the other arteries of the body, there is hardly any one which may 
not become the seat of an aneurism, but those of the popliteal artery are 
most common. 

STENOSIS. 

Stenosis and obliteration of the aorta, at the point of entrance of the 
ductus arteriosus, have been described in a considerable number of cases. 

The situation of the stenosis is either exactly at the entrance of the 
ductus arteriosus or close on either side of this point. The degree of 
stenosis varies". The aorta may be entirely closed and converted into a 
solid cord for a length of half an inch; or there may be a circular con- 
striction through which there is a larger or smaller opening — the con- 
striction is uniformly circular; or there is a septum springing from the 
concave side of the vessel at the opening of the ductus arteriosus; or 
there is a cicatricial-like contraction of the aorta. The walls of the 
aorta at this point may be thickened and sclerosed. The ductus arteri- 
osus may be closed or open. Above the constriction the aorta is usually 
dilated; below it, it is normal, dilated, or stenosed. 

Stenosis of the aorta produces hypertrophy of the left ventricle, and, 
later, of the right ventricle, with venous congestion ' throughout the 
body; or there may be a collateral circulation developed between the 
arteries given off above and below the constriction; or there may be rup- 
ture of the aorta, the right ventricle or auricle. 

This condition is found at all ages, but is produced during foetal life 






THE VASCULAR SYSTEM. 293 

or in the first year of extra-uterine life. It is probable that it may be 
caused after birth by an abnormal closure of the ductus arteriosus. 
This vessel normally becomes closed without the formation of a throm- 
bus. If a thrombus is formed, it may extend into the aorta and ob- 
struct it: or the ductus arteriosus is filled with a thrombus, but increases 
for a time in size; afterward, as the thrombus is absorbed, the vessel 
contracts and draws the walls of the aorta together. 

Stenosis of the aorta and of some of the other arteries has been ob- 
served, in a few rare cases, without any known cause. 

Endarteritis, with the production of atheromatous and calcareous 
patches, may obstruct or entirely obliterate the smaller arteries. This 
is especially seen in the arteries of the leg, foot, and brain, and in the 
coronary arteries. The writer (T. M. P.) has seen a case in which the 
subclavian was completely occluded in this way. 

Narrowing of the aorta and of all its branches, with thinning of the 
arterial coats, is found as a congenital condition. It usually occurs in 
females, in connection with imperfect development of the whole body. 

Stenosis from thrombosis or embolism is treated of elsewhere. 



RTJPTTJBES AND WOUNDS. 

Rupture of arteries may occur under the following conditions: 

1. Fatty degeneration or endarteritis, with atheromatous changes, 
may so soften and destroy the inner and middle coats of an artery as to 
admit of its rupture. The aorta, just above the valves, is the most fre- 
quent seat of this lesion. The rupture may run in any direction; its 
edges are irregular and jagged. The blood may burst through all the 
coats of the aorta at the same point; or, more frequently, the external 
coat remains and the blood is infiltrated in the middle coat and between 
it and the external coat. In this way, a dissecting aneurism is formed, 
which may extend along the aorta for a considerable distance. After a 
short time, the external coat usually gives way at some point, and the 
blood escapes. In rare cases, life is prolonged for some time, the rupture 
being closed by a new membrane. 

We also find ruptures from fatty degeneration and atheroma in the 
arteries of the brain and lungs; in the coronary arteries, the coeliac 
axis, the mesenteric arteries, and in the arteries of the extremities. 

2. In rare cases, stenosis of a portion of the aorta may cause rupture 
at some point between the seat of stenosis and the heart. 

3. Contusions, wrenchings, and severe falls may rupture the walls of 
an artery, either partially or completely, producing traumatic or dis- 
secting aneurisms, or completely severing the vessel. 

4. Penetrating wounds may injure or entirely sever an artery. If 
the vessel be large and the injury severe, death from hemorrhage is 



294 THE VASCTJLAK SYSTEM. 

the usual result. A small artery may become closed or be the seat of a 
false aneurism. 

In the healing of a wounded artery, two conditions co-operate. The 
vessel retracts and contracts, and a thrombus is formed within it. The 
contraction may be alone sufficient to close the vessel; its coats thicken, 
and the inner surfaces finally are fused together; or the blood coagulates, 
and forms a thrombus in the vessel near the wound. This thrombus 
later becomes organized, and the vessel is converted into a fibrous cord. 

Spurious or false aneurisms are found most frequently connected 
with vessels of the extremities. When an artery is wounded, the blood 
escapes into the surrounding soft parts, and a cavity is formed filled 
with blood and broken-down tissue. This condition may terminate in 
several ways. 

(a) The wound in the artery may heal and the effused blood be ab- 
sorbed. 

(b) The effused blood and broken tissues may become gangrenous and 
the surrounding soft parts be inflamed. 

(c) A sort of sac wall may be formed by the soft parts, while the 
wound of the artery remains open, so that we have an aneurismal sac 
through which the blood is constantly pouring. 

5. If an artery be wounded, and at the same time the vein which ac- 
companies it, we have as the result the conditions called aneurismal varix 
and varicose aneurism. In aneurismal varix, the artery and vein become 
adherent at the seat of injury, so that the arterial blood passes directly 
into the vein. There is a smooth, rounded opening between the two 
vessels, the vein is dilated into a sac, and the veins emptying into it are 
dilated and tortuous. 

In varicose aneurism, the artery and vein do not communicate di- 
rectly, but a false aneurismal sac is formed between the vessels, into 
which the blood is poured before passing into the vein. 

Varicose aneurism may also be produced by the spontaneous rupture 
of an aneurism into a vein. The aneurism presses against the vein, be- 
comes adherent, and finally ruptures into it. This condition has been 
observed between the aorta and pulmonary artery; the aorta and inferior 
and superior vena cava; the popliteal artery and vein; the femoral artery 
and vein; the splenic artery and vena azygos; the internal carotid and 
sinus cavernosus. Even in cases of perforation by aortic aneurisms, life 
is usually prolonged for some time. 

G. Destructive inflammation or tumors of the surrounding tissues 
may invade and destroy a portion of the wall of an artery. Thus ul- 
ceration of the trachea, bronchi, bronchial glands, and oesophagus, or 
tumors of these parts, may perforate the aorta; gangrene of the lungs, 
the pulmonary arteries; ulcer of the stomach, the gastric arteries, etc. 

Tumors. — Secondary tumors, chiefly carcinomata and sarcomata, 



THE VASCULAR SYSTEM. 295 

may occur in the walls of the arteries by continuous growth from with- 
out, involving first the external layers. To these layers they are usually 
confined, for the density of the inner layers affords such marked resis- 
tance to the infiltration of the tumor cells that they are apt to pass 
intact through the tumor which grows around them. More frequently 
the arteries become secondarily involved in the growth of malignant 
tumors by the occurrence, within them, of emboli formed by larger and 
smaller masses of tumor cells. 

These emboli are usually of small size, and are apt to get into the 
circulation by growing through the walls of the veins into their lumina^ 
Large emboli from tumors are most apt to occur in the branches of the 
pulmonary artery. The emboli, formed as they are for the most part by 
cells capable of growth and proliferation, are apt to soon form connec- 
tion with the walls of the vessels, and by the growth into them of blood- 
vessels from the vasa vasorum to find the conditions necessary for their 
development, and they may thus soon involve the entire wall of the ves- 
sel and grow out into adjacent parts. 



THE VEINS. 

DILATATION. 

Dilatation of the veins, or phlebectasia, presents itself under a va- 
riety of forms. 

1. Simple Dilatation. — The vein is uniformly dilated in a cylindri- 
cal or fusiform shape; its length is not increased; its walls are of normal 
thickness or thinned; the valves increase in size, or are insufficient, or 
atrophy, or are torn. 

2. Cirsoid Dilatation. — The vein is uniformly cylindrically dilated, 
but is also increased in length, so that it assumes a very tortuous course. 
The walls are normal, thickened, or thinned. 

3. Varicose Dilatation. — A circumscribed portion of the wall of the 
vein is dilated so as to form a globular sac. The sac communicates with 
the vein through a large or small opening. The wall of the sac is formed 
of the coats of the vein, which preserve their normal thickness, are thick- 
ened or thinned; the middle coat may disappear entirely. There may 
be only one such dilatation, or there may be a number on the same vein, 
or a number of veins may be affected at the same time. The vein may 
be otherwise normal, or, more frequently, is dilated in the cirsoid form. 

4. Anastomosing Dilatation. — A number of contiguous and anasto- 
mosing veins are dilated, both in the cirsoid and varicose forms. The 
vein then looks like a series of cavities separated by thin partitions. The 
dilatations of the same vein become adherent to each other and to those 
of the adjoining veins; portions of the wall of the dilated parts may dis- 



296 THE VASCULAR SYSTEM. 

appear, and we find a number of cavities containing venous blood, and 
separated from each other by thin partitions. The course of the vein 
can no longer be followed out. 

Spontaneous cure of dilatations of the veins is not common, and usu- 
ally occurs only in the lesser degrees of the lesion. Most phlebectasise 
increase steadily in size and extent. Very frequently thrombi form in 
the dilated veins, and either partially or completely fill them; and these 
in rare cases may become organized, or the clots may dry and become 
calcified, forming phleboliths (seepage 56), and, by the formation of new 
connective tissue in the walls, they may become inclosed in a fibrous 
capsule, with the obliteration of the vessel. The wall of the dilated sac 
may become so thin that it finally ruptures, and the blood is discharged 
externally. Sometimes inflammation is set up in the tissues surround- 
ing the vein, and we find both the surrounding tissues and the wall of 
the vein the seat of purulent infiltration or fibrous thickening. The 
parts of the body from which the dilated veins draw their blood may ex- 
hibit the results of chronic venous congestion, oedema, hyperasmia, and 
hypertrophy or ulceration. 

When occurring in mucous membrane, dilated veins are usually asso- 
ciated with persistent catarrh. There is hardly one of all the veins of 
the body which may not be dilated. The hemorrhoidal veins, the veins 
of the leg and thigh; those of the pelvis and pelvic viscera; those of the 
spermatic cord, scrotum, and labia; those of the abdominal wall; those 
of the neck and arms — are the ones most frequently found in this 
condition. ' 

The causes of dilatation are principally some mechanical obstruction 
to the passage of the blood through the veins towards the heart; but 
changes in .the walls of the vessels from inflammation or injury, etc., are 
not without influence. 

WOUNDS —RUPTURE. 

Wounds of the veins usually heal by a simple contraction and an ad- 
hesive inflammation of their walls : sometimes by the formation of a 
thrombus. Rupture of the veins may be produced by severe contu- 
sions and crushings of the body, and by violent falls. Perforation of a 
vein may be produced by suppuration of the soft parts, and the invasion 
of the walls of the vessel; by the pressure of an aneurism or of a new 
growth; by the thinning of the wall of the vein in phlebectasia. 

INFLAMMATION. 

Inflammation of the veins, phlebitis, may involve chiefly the external 
layers — periphlebitis; or the internal — endophlebitis ; or, as is very fre- 
quently the case, the entire wall may be affected. Phlebitis may be 
caused by the presence of a thrombus, by injuries, or by an inflammation 



THE VASCULAR SYSTEM. 



297 



of the surrounding tissues. Thrombosis of the vein, either primary or 
secondary, is a very constant accompaniment of phlebitis. 

Acute Phlebitis may commence as a suppurative periphlebitis or as a 
result of inflammatory processes about the vessel. The outer layers of 
the venous wall are congested, swollen, infiltrated with serum and pus. 
The inner coats may become infiltrated with pus; they may become ne- 
crotic and disintegrate. A thrombus is constantly formed under these 
conditions, which may for a time stop the circulation and keep the pro- 
ducts of inflammation and degeneration from mixing with the blood; but 
the thrombus itself is prone to disintegration, and thus the exudations 
and decomposing fragments of tissue may enter the circulation. 

On the other hand, owing to the presence of irritating or infectious 
material within the vein and the formation of a thrombus, the inflamma- 
tory process may be at the commencement an endophlebitis, but usually, 
if the inflammation be at all severe, the entire wall of the vessel will 




Fig. 151. 



-TUBERCULAR PHLEBITIS. 



The section is from one of the pulmonary veins in a child dead of acute general miliary tuber- 
culosis. Specimen loaned by Dr. W. P. Northrup. 

eventually be involved. The pus cells in both cases doubtless come from 
emigration from the vasa vasorum. Acute phlebitis may terminate in 
the absorption of the thrombus and the return of the vein to its normal 
condition; in the obliteration of the vein; or portions of the thrombus 
may become detached, and find their way as emboli into various parts of 
the body. The most important results of phlebitis are usually those 
which depend upon the introduction into the blood of these emboli or 
of septic material (see Thrombosis and Embolism, page 55, and Pyaemia). 

Chronic periphlebitis produces thickening, principally of the outer 
coats of the veins, but the inner coats may also be involved. The sur- 
rounding tissue may be also thickened and coalesce with the walls of the 
vein. There may or may not be thrombosis. 

Chronic endophlebitis is a not very common lesion, of the same gen- 
eral character as chronic endarteritis. More or less circumscribed 
24 



298 THE VASCULAR SYSTEM. 

patches of new connective tissue are formed in the inner coats, which 
may undergo fatty or calcareous degeneration. 

Tubercular Inflammation of the walls of the veins may occur as an 
extension of the process from without or from a lodgment of the 
tubercle bacilli in the blood current on the intima (Fig. 151). This is 
not infrequent in the pulmonary veins, and Weigert has recently called 
attention to the fact that in acute miliary tuberculosis the growth of 
tubercle tissue into the iumina of these veins from tubercular lymph 
nodes is of frequent occurrence, and readily explains the topography 
and mode of occurrence of the general disease. The tubercle bacilli 
which are present in the tubercular tissue growing into the lumen of the 
veins find thus an easy distribution. 

Syphilitic Inflammation may involve the walls of the veins either as 
gummy tumors or as more diffuse thickenings. 

TUMORS. 

Primary tumors of the veins are rare. Small leiomyomata have been 
described in the saphenous and ulnar veins. A myosarcoma as large as 
a man's fist has been described, situated in the dilated vena cava inferior. 
The veins are not infrequently secondarily involved by sarcomata and 
carcinomata, and sometimes by chondromata. The thin walls of the 
veins offer comparatively little resistance to the incroachment of malig- 
nant tumors, which thus gain access to the circulation and may form 
metastases in various parts of the body. 

PARASITES. 

Echinococcus is sometimes found in the veins, having either developed 
there or perforated from without. 

Two species of di stoma {liver fluke) occur in man. D. hepaticum 
occurs rarely in man, and while usually found in the bile ducts may occur 
in the vena cava. D. limmatobium is very common in man in Egypt and 
in other parts of Africa, and usually occurs in the portal vein or its 
branches, and frequently in other veins. 

THE CAPILLARIES. 

The walls of the capillaries are so thin and so intimately connected 
with the surrounding tissues that their lesions are studied most appro- 
priately among the diseases of the several organs. Dilatation of the new- 
formed capillaries in tumors, granulation tissue, etc. , and fatty and hyaline 
degeneration of their walls, may be mentioned here as readily observed 
lesions occurring under a variety of conditions. The changes which we 
assume to occur in the walls of the smaller veins and capillaries in exu- 
dative inflammation, by reason of which fluids and blood-cells pass 



THE VASCULAR SYSTEM. 299 

through them, are not yet sufficiently understood to be described with 
definiteness. 

THE LYMPH VESSELS. 

The smaller lymph vessels can hardly be treated as independent 
structures, since their walls are so closely joined with the tissues through 
which they pass; the lymph radicles, indeed, being nothing more than 
the spaces in the connective tissue in which the variously shaped con- 
nective-tissue cells lie. In the larger lymph vessels we find a moderate 
number of more or less independent lesions. 

INFLAMMATION. 

Lymphangitis. 

Inflammation of the larger lymph vessels is usually secondary, and 
connected with some wound or injury. Owing, it is believed, to the 
entrance into the lymph trunk of some septic material or bacteria, the 
vessels, sometimes for a considerable distance away from the wound, 
become red, tender, and painful. Under these conditions, the micro- 
scopical appearances which the vessels present vary. In some cases, the 
redness disappears after death, and we find no appreciable alteration. 
In other cases, we find the walls of the lymph vessels more or less densely 
infiltrated with pus cells, and the lumen may contain variable quantities 
of pus and fibrin and desquamated endothelium. The tissue about the 
vessels may also be infiltrated with serum and pus. These lesions may 
undergo resolution and the vessel be restored to its normal condition; 
or the vessel wall and surrounding tissue may die or become involved in 
abscess; or new connective tissue may form in and about the vessel, 
sometimes with obliteration of its lumen. The lymph nodes may par- 
ticipate in the inflammatory process. 

Inflammation of the lymph vessels may occur as the result of dissection 
and other wounds, and the bites of venomous reptiles. It may occur in 
the uterine lymphatics in the phlegmonous form of puerperal fever, and 
under other conditions. 

Tubercular Lymphangitis. — Tubercular inflammation occurs both in 
large and small lymph vessels. Miliary tubercles and diffuse tubercle 
tissue may form in the walls and project into the lumen of the larger 
trunks; or in the smaller vessels the new growth may entirely fill the 
lumen, and grow in this, with more or less involvement of the walls. 
This may occur independently, but it is most frequently seen in connec- 
tion with tubercular inflammation of adjacent tissues. Thus from tuber- 
cular lymph nodes in the vicinity of the thoracic duct there may be a 
direct extension of the tubercular inflammation, an involvement of the 
walls of the duct, and a growth of tubercle tissue into its lumen. 



300 THE VASCULAR SYSTEM. 

Such growths in the thoracic duct have been shown by Weigert to be 
frequent in acute general miliary tuberculosis, and very satisfactorily 
explain, on the hypothesis of the bacterial origin of the disease, the dis- 
semination of the tubercles. In the viciuity of tubercular ulcers in 
the intestines, furthermore, we often see the subserous lymph vessels, 
which pass from the vicinity of the ulcers, disteuded with the products 
of tubercular inflammation, and looking like dense white knobbed cords. 
Syphilitic Inflammation of the lymph vessels not infrequently occurs 
in the vicinity of syphilitic ulcers in the primary stage. In later stages 
there may be thickening of the walls of the vessels and the development 
of gummy tumors in and about them. 

LYMPHANGIECTASIS. 

Dilatation of the lymph vessels occurs under a variety of conditions. 
It may be congenital, or it may be due to some hindrance to the flow of 
lymph onward, as by pressure from any cause, or from the occlusion of 
the vessels by inflammation, or it may be produced by unknown causes. 
If the dilated vessels form a circumscribed mass, this is often called a 
lymphangioma (Fig. 67). In certain forms of elephantiasis and in 
macroglossia, the dilatation of the lymph vessels is an important factor. 
Its occurrence is not infrequent in the labia, prepuce, and scrotum. 

TUMORS. 

The relation of the endothelium of the lymph vessels and spaces to 
endotheliomata has been already mentioned in the section on Tumors. 

The dissemination of malignant tumors through the lymph channels 
is of frequent occurrence, and is particularly marked in the case of car- 
cinoma. In the vicinity of carcinomata, the lymph vessels are not infre- 
quently crowded with the tumor cells, forming white, irregular cords; or 
small masses of the tumor cells may be found in the lymph vessels, 
either near to or remote from the tumor. White, irregular networks are 
often formed in this way beneath the pleura in carcinoma of the lung 
(Fig. 71), or beneath the capsule of the liver. Transverse sections of 
lymph vessels thus distended show sometimes swelling and detachment 
of the endothelium and a crowding of the lumen with tumor cells. 
Whether or not the endothelium participates in the new formation of 
the characteristic carcinomatous cells is not known. 



THE LYMPH NODES (Lymph 

It is well, in studying the lesions of the lymph nodes, to remember 
that they are structures so placed in the course of the lymph vessels 

1 What we call lymphatic tissue embraces not only the so-called lymph glands and 
the less complex but still well-defined structures found in the stomach, intestines, 
tonsils, and elsewhere, and called lymph follicles, but also the less well-defined, 



THE VASCULAR SYSTEM. 301 

that the lymph, in flowing towards the larger central trunks, passes 
through them, undergoing a sort of filtration as it percolates through 
the trabecule of the lymph sinuses. If this simple fact be borne in 
mind, the diseases of the lymph nodes, which are, in the majority of 
cases, secondary, are much more readily understood. Particles of pig- 
ment which in any way get into the lymph vessels are carried along 
until a lymph node is reached, and here they are, in part at least, de- 
posited among the trabecules of the sinuses, while the lymph passes on 
and out of the efferent vessels (Fig. 154). The same thing occurs when 
cells from malignant tumors, bacteria of various kinds, etc., gain access 
to the lymph vessels, and also, as there is good reason for believing, in 
the case of many poisonous materials which our present knowledge does 
not enable us to associate with bacteria. These various materials, filtered 
out of the lymph by the glands, may act in a variety of ways to produce 
lesions in them. 

INFLAMMATION. 

Acute Inflammation of the lymph nodes usually occurs in connection 
with some inflammatory process in the region from which its lymph is 
gathered. The nodes are in the majority of cases swollen, reddened, 
and softer than normal, and often the seat of smaller and larger haem- 
orrhages. Sometimes one, sometimes several nodes of a cluster are 
affected. 

• The microscopical examination shows the most prominent change to 
be a great increase in the number of cells in the follicles and cords, as 
well as in the lymph sinuses. These cells are, in part, small and 
spheroidal, and similar to those normally filling the meshes of the folli- 
cles; in part, large polyhedral or variously shaped cells, with prominent 
nuclei; the latter cells are most abundant in the lymph sinuses (Fig* 
152). In addition to this, there is swelling of the endothelial cells of the 
reticulum of the sinuses. The blood-vessels may be distended with 
blood, or there may be blood, in greater or less quantity, free in the 
sinuses and follicles. The origin of the large number of new cells which 
may form in a very short time is not yet definitely known. They may 

irregular masses of tissue resembling that of lymph follicles, which, as Arnold has 
shown (Virchow's Archiv, Bd. 80, p. 315; Bd. 82, 394; Bd. 83, 289; Bd. 87, p. 114), 
is widely disseminated in variable amounts in different parts of the body; in the lungs,, 
beneath the pleura and elsewhere; in the liver, kidneys, etc. Although the exact 
nature of these more diffuse masses of lymphatic tissue is too little understood, as- 
indeed is that of the lymph follicles and glands themselves, there is reason to believe 
that they are analogous structures and prone to be affected by similar deleterious 
agencies. It seems better, in view of the fact that the so-called lymph glands are not 
glands at all, in the ordinary sense of the word, to call them lymph nodes, and the 
smaller masses of lymphatic tissue scattered through various parts of the body lymph 
nodules instead of " lymph follicles." 



302 



THE VASCULAR SYSTEM. 



be emigrated leucocytes or their derivatives ; they may be derivatives of 
the endothelium of the reticulum ; or they maybe in some cases, at least 
in part, cells which have been brought into the node, through the affe- 
rent trunks, from some external inflammatory focus. The capsule of the 
nodes, and not infrequently the connective tissue about them, may also 
be infiltrated with round cells. 

Acute inflammation may terminate in resolution, the new cells dis- 
appearing either by fatty or other degeneration, or by being carried off 
in the lymph, and the node return to its normal condition. This is the 
rule in the less intense forms of inflammation. On the other hand, the 
inflammatory process may become purulent and so intense as to lead to 
the formation of abscess, usually with a greater or less involvement of 
the tissue about the nodes. There may be at first numerous small ab- 




Fig. 152.— Acute Inflammation of Lymph Node in Typhoid Fever 
Showing a portion of one of the mesenteric nodes. A, capsule ; B, perifollicular space or 
lymph sinus, containing in its meshes many large cells; C, portion of one of the follicles, with large 
and small cells in the meshes of its reticulum. 



scesses which coalesce to form larger ones. These abscesses — buboes — 
may open externally or internally, or they may become dried and con- 
verted into cheesy masses which may calcify and, by a chronic inflam- 
mation in their periphery, become inclosed by dense connective tissue. 
Sometimes, instead of abscess being formed, the tissue of the inflamed 
nodes becomes necrotic and breaks down, inducing more or less severe 
inflammatory or necrotic changes in the tissues in their vicinity. 

In still other cases, acute inflammation of the lymph nodes passes 
into the chronic form. 



THE VASCULAR SYSTEM. 



303 



Moderate degrees of inflammation in the lymph nodes are very com- 
mon in connection with various forms of inflammation in neighboring 
parts Thus simple pharyngitis, gastro-enteritis, erysipelas, simple 
purulent inflammation, etc., are often associated with this lesion of the 
nodes. The lymph nodes of children are, as a rule, more easily affected 
by moderate inflammations in neighboring parts than are those of adults. 
Purulent inflammation of the lymph nodes is most frequently associated 
with severer forms of inflammation of adjacent or related parts, espe- 
cially those of an infectious character, syphilitic inflammation, poisoned 
wounds, pyaemia, etc. In a certain number of cases, we find bacteria in 
the inflamed lymph nodes, either singly or in zoogloea colonies, which 
have presumably something to do with the lesion. 




:;. v'y-;' 



:■, . - - -; 



IIP •"''" I ~:','' ; 'f-y \ f Mk ' 



Fig. 153.— Chronic Inflammation of Bronchial Lymph Node. 
Showing obliteration of the lymph sinuses and atrophy of the lymph follicles by the new-formed 
connective tissue. 

In many cases, the lesion of the lymph nodes appears to be induced, 
not by bacteria in the nodes themselves, but by ptomaines produced 
elsewhere by the action of bacteria and brought to the nodes by the 
lymph. The swelling of the lymph nodes in typhoid fever and diphtheria 
is probably induced in this way. 

Chronic Inflammation. — This is characterized by an increase of the 
connective-tissue elements of the node, with a gradual and commensurate 
disappearance of the lymphoid cells. The reticulum of the follicles and 
sinuses becomes thickened and fibrous, and in the trabecule and capsule 
new connective tissue is formed until, in advanced cases, the entire node 
may be more or less completely converted into a mass of connective 
tissue. This condition is very frequently seen in the lower tracheal and 



304 



THE VASCULAR SYSTEM. 



in the bronchial nodes, apparently as a result of the lodgment in them 
of respired pigment particles ; but it may occur in any nodes, either as 
a result of repeated moderate degrees of inflammation, or from causes 
which we do not know. In some cases, the nodes are greatly enlarged, 
and the new tissue contains many large cells,, while in other cases the 
connective tissue is dense and contains but few cells (Fig. 153). 

Pigmentation. — The pigment which is very frequently found in 
lymph nodes may be derived from the haemoglobin of the blood, either 
in the nodes themselves or in remote parts, or it may be formed of vari- 
ous materials introduced into the body from without, such as the pig- 
ments used in tattooing, respired dust particles of various kinds — coal, 
stone* iron, etc. (Fig. 154). The pigment particles, which usually first 




Fig. 154.— Pigmentation of Bronchial Lymph Node. 
The pigment is largely in the lymph sinuses and inclosed in cells. A, capsule of node : B, 
lymph follicle ; C, perifollicular lymph sinuses. 



lodge in the lymph sinuses, may collect here in large quantities, either 
in the reticulum or the cells lying in its meshes; they may penetrate 
the follicles and cords and find permanent lodgment there. They usually 
induce a greater or less degree of chronic inflammation, so that in ex- 
treme cases, such as are frequently seen in the bronchial lymph nodes, 
nothing is finally left of the node but a more or less deeply pigmented 
mass of dense connective tissue. The function of the node is, of course, 
in this way partially or entirely destroyed. The pigment in these cases 
appears to reach the node, in part by being carried along free in the 
lymph current, in part by becoming inclosed in leucocytes and being 
transported by them. Pigmentation of the nodes is most marked in 
those about the root of the lungs, which are frequently of a mottled 



THE VASCULAR SYSTEM. 305 

gray or a black color, but it may occur in the mesenteric and other nodes. 
Under similar conditions, the diffuse lymphatic structure in the lungs 
and liver may be similarly pigmented. 

Inflammation of the Lymph Nodes with Cheesy Degeneration. — This 
lesion of the lymph nodes, which is distinct from the above-mentioned 
comparatively infrequent cheesy degeneration of the contents of old ab- 
scesses, commences with changes similar to those above described in sim- 
ple inflammation. The node in this condition is swollen, and feels 
harder than normal; on section, it has a uniform reddish-gray color. 
Microscopical examination reveals a great increase in the number of 
parenchyma cells, some small and spheroidal, others large and poly- 
hedral. Sometimes the larger cells are multinuclear, and not infre- 
quently the reticular framework and the capsule are thickened. As the 
process advances, the characteristic necrotic changes make their appear- 
ance. We may find at first a greater or less number of the cells con- 
verted into a strongly retractile material, and the nuclei no longer 
capable of being stained. Then larger and smaller masses of cells 
undergo cheesy degeneration, with complete destruction of the blood- 
vessels, reticulum, and the spheroidal and other cells, and their conver- 
sion into a granular material. A section through the node in this con- 
dit'on shows the cut surface mottled with irregular-shaped, larger and 
smaller opaque white patches, which indicate the areas of cheesy degen- 
eration. These patches may increase in size and coalesce, so that a large 
part of, or even the entire gland may be converted into a more or less 
dense cheesy mass which may be surrounded by the thickened capsule. 

In this condition they may remain for a long time, and not infre- 
quently, owing to the involvement of a series of associated nodes, either 
simultaneously or one after another, and the increase of connective tis- 
sue about them, we find large, irregular nodular masses made up of a 
congeries of similarly affected nodes. 

On the other hand, the cheesy material may soften and break down, 
and, by the establishment of purulent and necrotic inflammation about 
them, abscesses may form which may open externally. These abscesses 
may heal; but usually the healing is difficult and slow, and long-contin- 
ued suppurations, frequently with the development of fistulae, are very 
common. Under these conditions, the inflammation may N assume a 
tubercular character. Instead of softening, the cheesy material in the 
glands may become dry and hard, and undergo calcification. 

Cheesy inflammation of the lymph nodes is most common in the cer- 
vical, bronchial, and mesenteric groups, but may occur anywhere. It is 
most apt to occur in badly nourished young persons, who, in addition 
to the lesion of the lymph nodes, are very liable to suffer from chronic 
inflammations of the mucous membranes, skin, periosteum, joints, and 
the subcutaneous and other connective tissues. This general condition 



306 THE VASCULAR SYSTEM. 

is known as scrofula, and the lesion of the nodes is sometimes called 
scrofulous inflammation. It is not infrequently associated with tuber- 
cular inflammation of the nodes, either as an independent lesion or as a 
part of a general tuberculosis, and by some writers tuberculous and 
scrofulous inflammation of the lymph nodes are considered to be identi- 
cal. In a considerable proportion of cases, however, of so-called scrofu- 
lous inflammation of the lymph nodes, there is no formation of tubercle 
tissue, and we find no tubercle bacilli, so that we must consider this 
class of cases as simply inflammatory, with a tendency to cheesy degen- 
eration. 

Tubercular Inflammation may occur in connection with simple in- 
flammatory changes in the lymph nodes, or with the form of inflamma- 
tion which tends to cheesy degeneration. It may be local, confined to 
the nodes, or it may occur in connection with general acute miliary 
tuberculosis or with tubercular inflammation of single organs. It may 
occur in single nodes or in several nodes of the same group, or in groups 
situated in different parts of the body. In its simple and acute form, 
there may be no evident change to the naked eye in the appearance of 
the nodes, or they may be besprinkled with small grayish-white, trans- 
lucent spots. Under these conditions, the nodes may be reddened and 
soft, or swollen and denser than normal. In more advanced forms of the 
lesion, the tubercles coalesce and undergo a greater or less degree of 
cheesy degeneration. Under these conditions, the cheesy areas are evi- 
dent to the naked eye as more or less sharply circumscribed opaque 
whitish areas, frequently surrounded by an irregular, more translucent 
grayish zone of tubercle tissue, which merges insensibly into the adjacent 
tissue. The entire node may become involved, and more or less com- 
pletely converted into a cheesy mass, in the periphery of which a zone 
of tubercle tissue may or may not be evident. 

Microscopically the small nodules or miliary tubercles are seen to con- 
sist of more or less circumscribed collections of small spheroidal, or more 
frequently larger polyhedral cells, with or without well-defined giant 
cells. They usually commence to form in the follicles and lymph cords 
of the nodes, and from these may spread and involve the entire sur- 
rounding tissue. The cheesy degeneration, which here as elsewhere is 
apt first to involve the central portions of the tubercles, presents the 
usual appearances. Tubercle bacilli may be found in the edges of the 
cheesy areas, or in the tubercle tissue about them. 

Simple inflammatory changes regularly occur in the periphery of the 
tubercles. There is an increase of cells in the lymph sinuses and follicles, 
and a more or less marked swelling, and apparently a proliferation of the 
cells of the reticular tissue of the node. In cases in which the process 
is chronic, there is often marked increase of the connective tissue of the 
nodes, the reticular tissue becomes dense and fibrous, and the trabecular 



THE VASCULAR SYSTEM. 



307 



•and capsule are thickened. The tubercles themselves, instead of under- 
going cheesy degeneration, may become fibrous or be converted into a 
hyaline material. 

The cheesy material may dry and shrink, and become inclosed by a 
capsule of dense connective tissue and become calcified; or it may soften, 
and thus cavities be formed in the glands, filled with grumous material; 
or inflammatory changes may be induced in the vicinity of the nodes, 
leading to abscesses. On the other hand, hyperplastic inflammation in 
the periphery of the affected nodes may result in their becoming bound 
together into a dense nodular mass. 

When cheesy degeneration has occurred, to the naked eye tuberculous 
lymph nodes may not be distinguishable from those in scrofulous in- 
flammation, but in some cases the nodular character of the new tissue 
around the cheesy centres is evident. The process is usually a slow and 
chronic one, except when occurring in connection with acute miliary 
tuberculosis in other parts of the body. It may occur in any of the 
nodes, but is most frequent in those of the bronchial, mesenteric, and 
cervical regions. 

Syphilitic Inflammation. — The lesions of the lymph nodes, which 
occur in connection with syphilitic poisoning, vary greatly, depending 
npon the stage of the disease. In the primary stage, the lymph nodes 
in the region of the seat of infection are apt to present the lesions of an 
ordinary acute inflammation, with a tendency to the assumption of the 
purulent form. 

In the secondary stage of the disease, the nodes of other regions, 
neck, elbow, axilla, etc., are frequently swollen and hard. On micro- 
scopical examination, there may be an increase of connective tissue in the 
capsule and trabecule, but the chief change is in the accumulation in tlie 
follicles and lymph sinuses of larger and smaller spheroidal and poly- 
hedral cells. The reticular tissue may be thickened, and the walls of the 
blood-vessels infiltrated with cells. In this condition the nodes may 
remain for a long time, not tending to form abscess; or they may undergo 
resolution through degeneration and absorption of the cells. 

In the tertiary stage of the disease, the nodes may be the seat of chronic 
inflammation characterized by the formation of gummy tumors. Under 
these conditions, they may form large, firm nodular masses by the grow- 
ing together by new connective tissue of several altered nodes. The 
gross and microscopical characters of gummata of the lymph nodes are, 
in the main, similar to those in other parts of the body. 

There are important changes in the lymph nodes which occur as 
local manifestations of general diseases, such as typhoid fever, leprosy, 
etc., which will be considered under the headings of these diseases. 

Degenerative changes in the lymph nodes, with the exception of those 
above described, are not of great frequency or significance. 



308 THE VASCULAR SYSTEM. 

Atrophy is a very regular occurrence in old age. In this condition, 
the nodes are small, hard, and, unless pigmented, white. Microscopical 
examination shows a marked diminution in the number of parenchyma 
cells, while the reticulum and the capsule and trabecule may be thick- 
ened. There may be an accumulation of fat around the node in con- 
nection with senile atrophy. 

It should be remembered, in this connection, that the lymph nodes, as 
well as the lymphatic tissue in general, in children are more voluminous 
and contain a greater number of parenchyma cells than in adults. 

Amyloid degeneration of the blood-vessels and reticulum of the 
lymph nodes occurs under the conditions which favor this change in 
general. It may occur in connection with amyloid degeneration of 
other parts of the body, or by itself. It may occur in nodes otherwise 
normal, or in those which are the seat of other lesions; thus in simple 
chronic or tubercular inflammation. It is frequently found in the 
mesenteric lymph nodes, in connection with waxy degeneration of the 
intestinal mucous membrane. 

Hyaline degeneration of the external layers of the smaller arteries and 
the capillaries of the lymph nodes, and also of the parenchyma cells, 
occurs occasionally in old age or in connection with wasting diseases. 
The vessels and cells are swollen and converted into a translucent, 
strongly refractile substance resembling amyloid optically, but not 
responding to its micro-chemical tests. By the accumulation of this 
material, the uninvolved parenchyma of the nodes may be compressed 
and atrophied. 

hyperplasia of the lymph nodes (Lymphoma). 

In addition to the considerable enlargements of the lymph nodes in 
inflammation which have been described above, they become enlarged 
under a variety of conditions which we do not understand. This lack 
of .knowledge of the etiology, together with our ignorance of the func- 
tion of the lymph nodes, and the morphological similarity, or even 
identity, which these enlarged nodes present, render it very difficult to 
decide upon the exact nature of the change, and in many cases to dis- 
tinguish one form from another. 

In the first place, there is a class of cases in which, sometimes 
slowly, sometimes with great rapidity, the lymph nodes of certain 
regions, especially the abdominal, axillary, cervical, and inguinal, en- 
large not infrequently to an enormous extent. They maybe either hard 
or soft, even almost fluctuating; the individual nodes may be distinct or 
merged into one another. Sometimes the nodes in nearly all parts of 
the body are affected. Microscopically we find that the enlargement is 
due, in the soft varieties, to an enormous increase of small spheroidal and 
polyhedral cells, and a growth of the reticular tissue. It is a new for- 



THE VASCULAR SYSTEM. 309 

matioQ of lymphatic tissue, but the normal relations of follicles, cords, 
and lymph sinuses is not preserved. In the harder varieties, there is a 
thickening of the reticular tissue in addition to an increase of cells. In 
very rare cases, portions of the nodes may become cheesy. Sometimes 
larger and smaller haemorrhages occur in the nodes, especially in the 
softer forms. In addition to these changes in the lymph nodes, there 
is, in a considerable proportion of cases, a new formation of lymphatic 
tissue in greater or less quantity in other parts of the body, in the spleen, 
in the gastro-intestinal canal, in the marrow of bones, in the liver, kid- 
neys, etc., and the number of leucocytes in the blood and in other parts 
of the body is increased. This general condition is known 'dsleukcemia, 
and will be considered under the general diseases. The enlarged lymph 
nodes in this disease may be called, for convenience, leuhmmic lymph- 
omata. 

In the second place, there is a form of disease in many respects, par- 
ticularly in the lesion of the lymph nodes, identical with leukaemia. 
There is, however, usually a less prominent involvement of the spleen 
and other lymphatic structures, and, what is more striking, no increase 
in the number of leucocytes in the blood. This is called Hodgkin's dis- 
ease, or pseitdo-leukcemia, and the enlarged lymph nodes may in this case 
be called pseitdo-leuhcemic lymphomata. The lesions of the lymph nodes 
are identical in both diseases, and it is convenient to assign different 
names to them simply because, for reasons which we do not at all under- 
stand, they seem to arise under different conditions, and to be associated 
with a constant difference in the character of the blood. 

TUMORS. 

Sarcomata occur in the lymph nodes as primary and secondary 
tumors, and these may be of various forms: spindle-celled, large and 
small round-celled, and angio-sarcomata. It is not easy in many 
cases to distinguish morphologically between the small round-celled sar- 
comata and the above-described lymphomata. Fibromata, myxomata, 
and chondromata occur in the lymph nodes, but are rare. Endothelio- 
mata are described, but are not common. Secondary carcinomata 
are of frequent occurrence, the form of the cells and the nature of their 
growth depending upon the seat and character of the primary tumors. 

PARASITES. 

Aside from various forms of bacteria which are not infrequently 
found in the lymph nodes — thus in diphtheria, splenic fever, typhoid 
fever, tuberculosis, etc.— filar ia, trichince, and pentastomum have been 
described. 



THE ALIMEISTTAKY CA^AL. 



THE MOUTH. 
MALFORMATIONS. 



Malformations of the lip and cheeks are usually associated with de- 
fective formation of the bones of the mouth. The entire process is gen- 
erally due to an arrest of development. 

1. The lower jaw is absent; the upper jaw and hard palate small and 
imperfectly formed; the temporal bones nearly touch in the friedian line. 
The lower part of the face is, therefore, wanting; the mouth is absent, or 
small and closed posteriorly; the tongue is absent. Such a malforma- 
tion is rare; the fo&tus is not viable. 

2. The face remains in its early foetal condition of a large cleft; 
the mouth and nose form one cavity; the orbits may be united in the 
same cavity. The foetus is not viable. 

3. There is a cleft in the upper lip, upper jaw, and hard palate. 
The cleft corresponds to the point of junction of the processes of the 
superior maxilla with the intermaxillary bone. There may be one cleft 
or two, one on either side of the intermaxillary bone. The cleft involves 
the lip alone, or the lip and superior maxilla, or the lip, maxilla, and 
palate. There may be a single or a double cleft in the palate; and the 
cleft may involve either the hard or soft palate, or both. If there are 
two clefts of the lip and maxilla, the portion of lip and bone between 
them may be small, or entirely absent, so as to leave a large open space. 
The soft palate may be entirely absent. This is a common malforma- 
tion, and does not endanger life. 

4. Rarely we find a cleft involving the middle of the lower lip, and 
sometimes extending into the inferior maxilla. 

5. Either the inferior, the superior, or both maxillary bones may be 
abnormally small. 

6. The edges of the lips may be partly or completely joined together. 
The opening of the mouth may be only a round hole. 

7. The lips may be absent or imperfectly developed. 



THE ALIMENTARY CANAL. 311 

8. The corners of the mouth may be prolonged by clefts in the 
cheeks nearly to the ears. 

HYPERTROPHY. 

The skin of the cheeks and lips may be hypertrophied in connection 
with elephantiasis of the face. 

There may be a thickening of the lips alone, so that they appear dou- 
ble. This thickening may be due to an increase of all the anatomical 
elements of the lips; or there may be an increase and dilatation of the 
lymphatic vessels, giving to the growth a soft, (edematous character. 

INFLAMMATION. 

Catarrhal Stomatitis is found most frequently in children. It is pro- 
duced by a great variety of local and constitutional causes. Of the con- 
ditions which are seen during life, the congestion, increased production 
of mucus, and swelling of the mucous membrane, but little remains after 
death. 

Duriug life, the congestion and swelling of the mucous membrane 
are well marked. There are often white patches, produced by the death 
of the superficial epithelial cells. There may be an increased production 
of mucus, which runs constantly from the mouth, or, instead of this, the 
entire mucous membrane is unnaturally dry. 

The only structural changes which can be demonstrated are the de- 
generative changes of the epithelial cells and the production of pus glo- 
bules, which infiltrate to a moderate degree the stroma of the mucous 
membrane and appear on its surface. 

Croupous Stomatitis is produced by local irritants, b}^ extension of 
the same form of inflammation from the pharynx, and it occurs with the 
exanthematous fevers and with diphtheria. 

Portions of the mucous membrane are swollen and congested, and 
covered with a false membrane. This false membrane is composed of a 
thickened layer of epithelium in the condition of coagulation necrosis, 
and of fibrin and pus in variable relative quantity. The stroma of the 
mucous membrane is infiltrated with pus and fibrin, and portions of it 
may become necrotic. 

stomatitis ulcerosa ' (Stomacace; Stomatite Ulcer o-membraneuse). 

This form of stomatitis occurs in children between the ages of four 
and eight years, and in adults between the ages of eighteen and twenty- 
five years. It is apt to occur in localized epidemics, in hospitals and 
asylums, and among soldiers and sailors. Some of the forms of mercu- 
rial stomatitis seem to be identical with this form of inflammation. 



zvon, "Stomatite ulcerosa." Union Medicale, 1859. Bohn, " Mund- 
krankheiten der Kinder," 1880. 



312 THE ALIMENTARY CANAL. 

The inflammation begins at the margin of the gums of the lower 
jaw. The gums are swollen and coated with a grayish, soft matter, 
composed of bacteria and detritus. Then follows destruction of tissue; 
the gums are destroyed around the teeth, and these fall out; the inflam- 
mation extends to the lips, cheeks, and tongue. The ulcers are coated 
with a thick, soft, gray membrane. The surrounding soft parts are 
swollen, and there may be necrosis of the jaws. 1 

Syphilitic Stomatitis. — As a result of syphilis, there maybe produced 
either the so-called mucous patches or gummy tumors. In the mucous 
patches, we find at first the epithelial layer thickened and the papillae 
of the stroma swollen and infiltrated with cells. This may be followed 
by desquamation of the epithelium and ulceration of the stroma. 

The deeper gummy tumors may also soften and form ragged ulcers 
of some size. 

Tubercular Stomatitis commences with the formation of miliary 
tubercles or of larger tubercular masses in the stroma of the mucous 
membrane. These masses soon degenerate, soften, and form ragged 
ulcers resembling very closely syphilitic ulcers. 

GANGRENE. 

Gangrene of the lips and cheeks, or noma, is most frequent in ca- 
chectic children as a consequence of the abuse of mercury. Much more 
rarely it occurs in adults after typhus and other exhausting diseases. 
The disease begins in the mucous membrane of the cheeks near one of 
the corners of the mouth. The mucous membrane becomes black and 
gaugrenous; the gangrene extends rapidly through the entire thickness 
of the cheek, and produces perforation; it extends laterally in all direc- 
tions. 

TUMORS. 

Adenomata are formed in the mucous membrane covering the mouth, 
lips, and soft palate. The tumors are rounded, usually small, some- 
times as large as a hen's egg. They may be situated in the thickness of 
the mucous membrane, or project in a polypoid form. They are formed 
by an hypertrophy of the normal mucous glands. The glandular acini 
are increased in number and size, the epithelial cells are increased in 
number and may undergo colloid degeneration. 

Papillomata occur most frequently at the edges of the lips, but are 
also found on the gums, the floor of the mouth, and the cheeks. They 
are formed of hypertrophied papillae, covered with thickened epidermis. 
They very often ulcerate. 

1 B. Volkmann, Yirch. Arch., Bd. 50, p. 142, describes five cases of inflammation 
of the mucous glands of the lower lip. The lip was swollen and hard, the mucous 
glands and their ducts were dilated. 



M 



THE ALIMENTARY CANAL. 313 

Carcinomata are of frequent occurrence. They may be found at any 
part of the mucous membrane of the mouth, but as a rule begin in the 
edge of the lower lip. 

They may originate in an ulcerating papilloma, or as a flat, super- 
ficial growth from the deeper layers of the epithelium, or as deep 
nodules starting in the mucous glands. They are composed of large 
masses of epithelial cells, closely packed together, often forming nests, 
and arranged in anastomosing tubular masses. The stroma surrounding 
these masses is infiltrated with cells. In a few cases the infiltration of 
the stroma with small round cells may be very marked, so marked that 
the epithelial growth may be obscured. The new growth increases in 
size, ulcerates, infiltrates the adjacent tissues, and may give rise to metas- 
tatic tumors. 

Angiomata are found in the lips. They may be congenital or devel- 
oped after birth. 

Fibromata, lipomata, and enchondromata have been seen in a few 
cases in the lips. When they appear in the mouth they usually grow 
from the bones. 

THE TONGUE. 

MALFORMATIONS. 

Absence of the tongue is found in connection with the extreme de- 
fects of development of the face already mentioned. 

The anterior portion of the tongue may be absent while its base re- 
mains. The lower jaw is then small. 

The tongue may be partly or completely adherent to the floor of the 
mouth. The frenulum may be abnormally short, or may extend to the 
tip of the tongue. In rare cases, the sides of the tongue are adherent, 
or its upper surface may be adherent to the roof of the mouth. 

HYPERTROPHY. 

Macroglossia, or hypertrophy of the tongue, is almost always a con- 
genital lesion, and is especially common in cretins. The tongue is so 
large that the cavity of the mouth cannot contain it; it is protruded 
through the lips and displaces the jaws. The lips may also be hypertro- 
phied in the same way. 

There is an hypertrophy of all the anatomical elements which make 
up the tongue, and in addition to this there may be a dilatation of the 
lymphatic vessels. 

INFLAMMATION. 

Inflammations of the tongue may be associated with similar changes 
in the mouth, or may occur by themselves. 

Superficial Glossitis. — Inflammation involving only the mucous 
membrane of the tongue may occur as an acute or chronic process. 
25 



314 THE ALIMENTARY CANAL. 

The acute forms present no marked lesions. 

The chronic forms result in an increased production of epithelium 
and an hypertrophy of the papillae of the tongue. 

A moderate development of such an inflammation is not infrequently 
associated with derangements of the stomach. The tongue is large, its 
surface is irregular from the hypertrophy of the papillae. There may be 
no change in the epithelium, and then the surface of the tongue is clean 
and red ; or the epithelium is increased and the tongue is covered with 
a white fur. 

More severe forms of the disease also occur, especially with syphilis. 
The hypertrophied papillae and increased epithelium then alter very de- 
cidedly the appearance of the tongue. 

Parenchymatous Glossitis may be produced by mercurial poisoning, 
by injury, or by unknown causes. The tongue is swollen, the muscular 
and connective portions are congested and infiltrated with serum and 
pus. The inflammation may stop at this point, or it may go on to the 
formatiou of an abscess. 

Syphilitic Glossitis. — In persons suffering from constitutional syphi- 
lis there may be mucous patches on the surface of the tongue; or 
gummy tumors in its stroma, which often soften and form deep ulcers ; 
or a diffuse, chronic inflammation of the surface of the tongue, with 
hypertrophy of the papillae. 

Tubercular Glossitis. — There may be a tubercular inflammation of 
the connective tissue of the tongue just beneath the epithelial layer, re- 
sulting in the formation of tubercle granula and granulation tissue. In 
this way tumors of some little size are formed, which may remain un- 
changed for some time, or may degenerate, soften, and form ulcers. 

TUMORS. 

Cysts. — The most common forms of cysts are the sacs beneath or 
partly in the substance of the tongue (ranula). They are formed by 
dilatation of the ducts of the submaxillary and sublingual glands; or 
make their appearance in the connective tissue beneath and in the 
tongue. 

Angioma. — Cavernous vascular tumors are found in the substance of 
the tongue and projecting from its surface. 

Lipoma and fibroma are rare. They form nodules in the substance 
of the tongue, or project in a polypoid form. Composite tumors, com- 
posed largely of fat, are found in the tongue as a congenital condition. 

Lupus occurs in the form of nodules and ulcers at the base of the 
tongue. 

Sarcomata are rare in this situation. I (Delafield) have seen one 
such tumor in a young child. It formed a nodule as large as a chestnut, 
and was composed of round and fusiform cells. 



THE ALIMENTARY CANAL. 315 

Carcinoma. — This form of new growth may begin in the tongue or 
may extend to it from the adjacent tissues. The growth is composed of 
large, flat epithelial cells packed closely together in anastomosing tubular 
spaces and surrounded by a connective-tissue stroma. 

THE PHARYNX AND THE (ESOPHAGUS. 
MALFORMATIONS. 

Fistulous openings from the pharynx, running between the muscles 
and perforating the skin, have been seen in rare instances. These 
fistulse are so small as to have no practical interest. 

The oesophagus may be entirely absent, or its lower portion may be 
present and joined to the pharynx by a solid cord; or the pharynx, or 
the lower part of the oesophagus, may be continuous with the trachea; 
or the entire oesophagus. may be represented by a solid cord. 

Diverticula of the pharynx, dilatations of the oesophagus, and 
division of the middle portion of the oesophagus into two branches have 
all been observed. 

INFLAMMATION. 

Catarrhal and Croupous Pharyngitis are usually associated with 
the same forms of inflammation in the mouth, and have the same char- 
acters. 

Submucous Pharyngitis may occur with inflammations of the mucous 
membrane, with caries of the cervical vertebrae, with inflammation of 
the cervical and parotid glands, with periostitis of the cranial bones, or 
maybe idiopathic. It may result in swelling and oedema, in induration, 
or in suppuration. It is most important when it affects the posterior 
wall of the pharynx and forms retro-pharyngeal abscesses. Such ab- 
scesses may cause death by suffocation. 

Catarrhal Oesophagitis may be either acute or chronic. The chronic 
form may produce ulceration, or relaxation and dilatation of the walls, 
or hypertrophy of the muscular coat. 

Croupous Oesophagitis is found with- croup of the pharynx, and after 
the exanthemata and other severe diseases. 

Irritating and caustic acids and alkalies destroy larger or smaller 
portions of the mucous membrane. The necrosed portions are of a 
black or whitish color, surrounded by a zone of intense congestion. If 
the patient recover, the patches of membrane which have been destroyed 
slough, fall off, and leave a granulating surface. In this way, dangerous 
stenosis of the oesophagus may be produced. 

Foreign bodies which are swallowed and become fixed in the oeso- 
phagus cause inflammation of the mucous membrane and of the adjoin- 
ing soft parts. The inflammation may go on to produce abscesses 



316 THE ALIMENTARY CANAL. 

around the oesophagus, or to destroy the wall of the canal, and the 
foreign body finds its way into the trachea, aorta, or pericardium. 

Inflammation of the submucous tissue of the oesophagus, apart from 
the cases just mentioned, is not common. It may cause the formation 
of abscesses, or of fibrous tissue, which may produce stenosis. 

ULCERATION. 

Ulceration of the pharynx occurs in rare cases as the result of catar- 
rhal inflammation. More frequently it is produced by syphilis, either 
in the form of superficial ulcers or of deep and extensive destructions of 
tissue from the softening of gummy tumors. 

Lupus also sometimes attacks the upper part of the pharynx, and 
produces extensive ulceration. Ulceration of the oesophagus is not com- 
mon, but a few cases of simple perforating ulcer have been described. 1 

Foreign bodies in the oesophagus may perforate its wall, as already 
mentioned. Perforation of the oesophagus from without may be pro- 
duced by inflamed bronchial glands, by cavities and gangrene of the 
lungs, by abscesses in the mediastinum, by abscesses accompanying 
caries of the vertebrae, and by aneurisms of the aorta. Oases have been 
described of rupture of the wall of the oesophagus by violent coughing 
and vomiting, but it seems probable that there was really some previous 
disease to account for the rupture. 



Simple cylindrical dilatation of the oesophagus is usually the result 
of long-continued stenosis of the oesophagus or of the cardiac end of the 
stomach; although not nearly all the stenoses are followed by dilatation. 
These dilatations are formed at first immediately above the stenosis and 
then extend upward. Only in rare cases does the dilatation involve 
the whole length of the tube. The entire wall of the dilated portion of 
the oesophagus is thickened, and there maybe polypoid outgrowths from 
the mucous membrane. 

In rare cases there is cylindrical dilatation of part or of the whole of 
the oesophagus without a stenosis or any discoverable cause. In these 
cases the dilatation is usually greatest near the middle of the oesophagus 
and diminishes upward and downward, so that the oesophagus has a 
fusiform shape. The dilatation may reach a very considerable degree, 
the walls of the oesophagus are thickened, its mucous membrane may be 
covered with papillary outgrowths or ulcerated. 

The Sacculated Dilatations of the oesophagus are of two kinds: those 
due to pressure, and those due to traction. 

1 Graefe u. Walther, Jour. f. Chir. u. Augenkeilk. , Bd. 19. Med. Chir. Trans., 
Vol. 36. Bokitansky, "Path. Anat." 

-Ziemssen, " Cyclopaedia of Medicine," viii., p. 47. 



THE ALIMENTARY CANAL. 317 

The dilatations due to pressure are situated in the posterior wall of 
the pharynx, just at its junction with the oesophagus. The smaller sacs 
are from the size of a pea to that of a hazelnut; the larger sacs may 
reach an enormous size, and hang down between the oesophagus and the 
vertebral column, the opening into the oesophagus remaining compara- 
tively small. It is supposed that a limited area of the wall of the oeso- 
phagus loses its power of resistance against the pressure exercised upon 
it in each act of swallowing; it then is forced outward by the pressure, 
and so there is formed first a protrusion and then a sac. When a sac is 
formed, the food enters it, accumulates there, and so the sac becomes 
larger and larger. 

The dilatations due to traction are situated on the anterior wall of 
the oesophagus, at a point nearly corresponding to the bifurcation of the 
trachea. They are of funnel shape, with the small end outward. Their 
length varies from two to twelve millimetres; the width of the opening 
into the oesophagus is from six to eight millimetres. 

These dilatations are due to inflammation of the parts adjoining the 
oesophagus, especially of the bronchial glands, followed by adhesions to 
some part of the anterior wall of the oesophagus. These adhesions then 
contract and draw the wall of the oesophagus outward, and in this way 
the dilatations are formed. 

At a later time these sacs may perforate into the bronchi, the lungs, 
the pleural cavity, the pericardium, the aorta or pulmonary artery. 

STENOSIS. 

Congenital Stenosis. — Besides the defects of development of the oeso- 
phagus which are incompatible with life, there may be a congenital ste- 
nosis of some part of it which causes difficulty in swallowing, but yet 
does not destroy life. 

Stenosis by Compression is not uncommon. Tumors of the neck 
and mediastinum, and aneurisms of the aorta, are the usual causes. 

Stenosis by Obstruction. — Foreign bodies may be lodged in the oeso- 
phagus. Tumors may hang down from the pharynx into the oesopha- 
gus, or may be situated in the wall of the oesophagus. Inflammation of 
the oesophagus, due to the ingestion of irritating poisons, produces cica- 
tricial stenoses. A few cases of stenosis due to syphilitic inflammation 
have been reported. 

TUMORS. 

The veins of the oesophagus may be enormously dilated. They may 
rupture, and so give rise to haemorrhage. 1 

Cysts. — Small retention cysts of the follicles of the mucous mem- 

1 Bristowe, Trans. London Path. Soc, 1856. 



318 THE ALIMENT AET CANAL. 

brane are sometimes found. Van Wyss 2 describes a cyst as large as an 
apple attached to the posterior wall of the oesophagus, one and one-half 
inches above the stomach. It was filled with ciliated epithelium. 

Papillomata of small size may be found in considerable numbers 
throughout the entire length of the oesophagus, or may occur singly. 
Large papillary tumors are more rare. 

Fibromata grow from the periosteum of the bones at the base of the 
skull, and project into the cavity of the pharynx and posterior nares in 
the form of large polypoid tumors. Small fibrous tumors are formed in 
the submucous connective tissue of the oesophagus. Tumors, which at- 
tain a very large size, originate in the submucous connective tissue on 
the anterior wall of the lower part of the pharynx, and as they grow hang 
down into the oesophagus. 

Lipomata of small size are sometimes found in the wall of the oeso- 
phagus. 

Myomata composed of smooth muscle may grow in the muscular coat 
of the oesophagus and attain a considerable size. 2 

Carcinomata may originate at any part of the wall of the pharynx and 
oesophagus. They are composed of flat epithelial cells closely packed 
together in masses in the usual way. In the oesophagus, the new growth 
begins in the deeper layers of the mucous membrane, and grows so as to 
encircle the tube for a length of one or more inches. The tumor remains 
as a flat infiltration, or it ulcerates, or it projects inward in large fun- 
gous masses. The growth may extend up and down the oesophagus and 
even involve the pharynx or stomach. 

The ulcerative process may extend outward so as to produce perfora- 
tion into the air passages, the lungs, pleurae, pericardium, and large blood- 
vessels. 

The new growth may extend outward and infiltrate the surrounding 
soft parts, so that the oesophagus is surrounded by large, solid, cancerous 
masses. Metastatic tumors are also sometimes formed. 

Adenoma. — A polypoid adenoma composed of tubules lined with cylin- 
drical epithelium, and growing from the anterior wall of the oesophagus, 
has been described by Weigert. 3 

I (Delafield) have seen one tumor, the size of a chestnut, growing 
in the soft palate, which was composed of a stroma of connective and 
mucous tissue in which were irregular, anastomosing tubules filled with 
small, polygonal, nucleated cells. It could be called an adenoma or a 
carcinoma. 



^irch. Arch., Bd. 51, p. 143. 

2 Virch. Arch., Bd. 43, p. 137. Med. Times and Gazette, Nov. 28th, 1874. 
Glasgow Med. Journal, Feb., 1873. 
3 Virch. Arch., Bd. 67, p. 516. 



THE ALIMENTARY CANAL. 319 

Another composite tumor grew from the mucous membrane of the 
pharynx behind the left tonsil. It filled the pharynx below the level 
of the palate. It had the gross appearance of a myxo-sarcoma, the cen- 
tral portions being very soft. It was composed of connective tissue, 
mucous tissue, fat, sarcomatous tissue, and irregular tubules lined with 
small, polygonal epithelial cells. Some of the tubules were distended 
with masses of hyaline matter. The whole structure resembled that of 
the tumors so often found in the parotid region — tumors which can be 
called '' adenoid myxo-sarcomata." 

Sarcoma. — I have seen one case in which there was a diffuse growth 



Fig. 155. — Diffuse Sarcoma of the Pharynx, x 850 and reduced. 

involving both the tonsils, the posterior and lateral walls of the pharynx, 
the base of the tongue, and the epiglottis. The new growth replaced the 
mucous membrane, infiltrated the soft parts for a short distance, and 
projected inward in polypoid masses. It was composed of small, poly- 
gonal, nucleated cells, contained in a very delicate nucleated stroma 
(Fig. 155). 

THE STOMACH. 

MALFORMATIONS. 

Malformations of the stomach are not common. The organ may be 
entirely wanting in acephalous foetuses. It may be of various degrees of 



320 # THE ALIMENTARY CANAL. 

smallness, sometimes no larger than the duodenum. It may be divided 
into two halves by a deep constriction in the middle. The pyloric orifice 
may be stenosed or entirely closed. The stomach may be outside of the 
abdominal cavity from a hernial protrusion through the diaphragm, or 
at some point in the abdominal wall. It is found on the right side, in- 
stead of the left, when the other viscera are transposed, and the position 
of the cardiac and pyloric orifices is correspondingly inverted. 

POST-MORTEM CHANGES. 



In adults, the stomach after death is of a grayish or pinkish color, 
sometimes mottled with red ecchymoses. The mucous membrane is 
soft, and the epithelium easily brushed off. At the fundus the food is 
usually found collected, and here the mucous membrane is the softest. 
It is very common to find the epithelium removed from the entire fun- 
dus of the stomach, so that all that portion of its wall is grayer and 
thinner, there being a sharp dividing line between the two portions. 
Sometimes this post-mortem softening process goes on to destroy all the 
coats of the stomach, and even the adjoining portion of the diaphragm. 
In this way, the* contents of the stomach may be emptied into the pleural 
cavity by a large, ragged opening in the stomach and diaphragm. When 
the softening affects all the coats of the stomach, the softened portion is 
not sharply limited. The entire thickness of the affected portion of the 
wall is converted into a gray or yellow semi-transparent jelly, or into a 
blackish, broken-down pulp. 

This softening is most frequent in children, but also occurs in adults, 
usually in connection with severe and exhausting diseases. 

A similar post-mortem softening of the wall of the oesophagus has 
been described by Moxon. 1 

INJURIES. 

Perforating wounds of the stomach usually give rise to a fatal perito- 
nitis. It is possible, however, for the wound to heal, or a gastric fistula 
may be formed. 

Rupture of the stomach may be produced by severe blows or falls. 

HAEMORRHAGE. 

Small extravasations of blood in the wall of the stomach are frequently 
found in persons who have died from one of the infectious diseases. 

Haemorrhage into the cavity of the stomach may be produced in a 
variety of ways. 

In ulcers of the stomach, there may be bleeding from the small ves- 
sels of the ulcer, or from the perforation of a larger artery. 

In cancer of the stomach, there may be bleeding from the tumor. 

1 Trans. Lond. Path. Soc, 1870, p. 159. 



— 



THE ALIMENTARY CAN AX. 321 

Some cases of chronic gastritis are characterized by general bleeding 
from the mucous membranes of the stomach. 

Cirrhosis of the liver is not infrequently attended with large haem- 
orrhages from the mucous membrane of the stomach. 

Small aneurisms of the arteries in the wall of the stomach may rup- 
ture internally. 

In yellow fever and some of the other infectious diseases, there is 
haemorrhage into the cavity of the stomach. 

Patients may vomit blood during life, and after death no lesion to 
account for the bleeding be found. 

INFLAMMATION. 

Acute Catarrhal Gastritis, as we see it after death, is usually due to 
the ingestion of irritating substances, or forms part of the lesions of 
cholera morbus. If we can judge from clinical symptoms, it occurs 
during life as a temporary condition from a variety of causes. 

After death the mucous membrane is found congested and swollen, 
or the congestion may have disappeared. The mucous membrane is 
coated with an increased amount of mucus, especially at the pyloric end 
of the stomach. Sometimes there are a number of minute white dots 
in the substance of the mucous membrane. 

The structural changes in the mucous membrane consist simply in a 
swelling of the cells of the gastric tubules, a slight infiltration of the 
stroma with pus cells, and a swelling of the patches of lymphatic cells. 
The little white dots, when they are present, are composed of small foci 
of pus between the gastric tubules, with degeneration and destruction of 
some of the tubules. 

Chronic Catarrhal Gastritis is a very common disease. There is, 
however, no very close relation between the severity of the symptoms 
during life and the extent of the lesions found after death. 

In some cases, chronic alcoholism, or the abuse of drugs, or the mode 
of life of the patient seems to be the cause of the lesion. Chronic 
phthisis, chronic Bright's disease, cirrhosis of the liver, and fatty liver 
are often accompanied by chronic gastritis. Organic disease of the heart, 
or pressure on the ascending vena cava, produces a form of chronic gas- 
tritis characterized by intense general congestion. 

After death the stomach is found either empty or still containing 
food. It is of normal size, or dilated, or small, sometimes hardly larger 
than the duodenum. Its inner surface is coated with a thick layer of 
tenacious mucus, most abundant at its pyloric end. The mucous mem- 
brane is congested, or white, or slate colored, or mottled with small white 
spots. It is of normal thickness, or thinned, or thickened, or there are 
little polypoid projections from its surface, or there is cystic dilatation 
of the gastric tubules. The connective tissue and muscular coats remain 



322 THE ALIMENTARY CANAL. 

unchanged, or they are thinned and relaxed, or they are hypertrophied. 
The hypertrophy may be diffuse, or it is confined to the pyloric end of 
the stomach and may then produce stenosis of the pylorus. 

The minute lesions consist principally in changes in the mucous 
membrane. The cells of the gastric tubules are swollen, degenerated, 
and broken down. The tubules are atrophied and deformed, or dilated 
into cysts. The patches of lymphatic tissue about the blind ends of the 
tubules are increased in size. The connective tissue between the tubules 
is infiltrated with cells and increased in quantity. 

Croupous Gastritis is of rare occurrence. It is found in children 
with croupous inflammation of the pharynx and oesophagus, and is then 
usually in small patches. In adults, it is almost always secondary to 
typhus, pyaemia, puerperal fever, cholera, dysentery, the exanthemata, 
and irritating poisons. The false membrane is in small patches, or may 
line a large part of the stomach. The disease is usually not diagnosti- 
cated during life, the symptoms of the primary disease diverting atten- 
tion from the gastritis. 

I (Delafield) have seen one case of idiopathic croupous gastritis in an 
adult. A man, forty-six years old, was in good health until eight days be- 
fore his death. At that time he caught cold, had pains over his bowels, 
tenderness over the liver, constipation, cough with mucous expectoration, 
temperature 102-| o , pulse 120. On the day of his death, the eighth day 
of the disease, the temperature was 100°, pulse 112, tongue dry, abdo- 
men tympanitic and tender, and he died in a prolonged attack of syn- 
cope. At the autopsy all the viscera were examined. Excepting evi- 
dences of bronchitis in the lungs, there were no lesions save in the 
stomach. About two-thirds of the internal surface of the stomach, in- 
cluding the lesser curvature and anterior and posterior walls, appeared 
to be covered with a thick false membrane, which did not quite reach 
to the cardiac or pyloric orifices. Minute examination showed that 
there was a layer of exudation on the internal surface of the mucous 
membrane. This exudation consisted of fibrillated fibrin and lymphoid 
cells dipping into the mouths of the follicles. Beneath the exudation 
the mucous membrane was thickened and altered. A large number of 
lymphoid cells separated the follicles, and even replaced them entirely. 
The submucous layer was very much thickened by the presence of 
lymphoid cells, fibrillated fibrin, and fibrous tissue. The muscular coat 
was separated into layers by groups of lymphoid cells. 

Wilks and Moxon 1 mention a similar case in a man with chronic 
B right's disease; and a case of both croupous gastritis and colitis with 
abscess of the liver. 

Suppurative or Phlegmonous Gastritis. — A formation of circum- 

1 "Path. Anat.," p. 381. 



THE ALIMENTARY CANAL. 323 

scribed collections of pus may occur in the connective-tissue coat of the 
stomach, as it does in other parts of the body, in puerperal fever and the 
infectious diseases. 

Idiopathic suppurative gastritis is a disease of rare occurrence. 
Leube 1 has collected 31 cases, of which 26 were males and 5 females. 
In some of the cases the inflammation was ascribed to the excessive use 
of alcohol, in others to a wound in the region of the stomach, in others 
to some error in diet. 

Fagge 2 describes a case in a male of fifty-one years of age, without 
discoverable cause. 

Silcock 3 describes a case in which the gastritis followed the operation 
of gastrostomy. 

I have seen one case occurring in an adult male, without any known 
cause. 

The suppurative inflammation seems to begin in the connective-tissue 
coat of the stomach. From thence it may extend to the glandular coat 
and produce perforations, or outward to the muscular and peritoneal 
coats. In some cases there is added a local or general peritonitis. 

The inflammation may involve one or more circumscribed areas and 
so produce abscesses, or it may be a diffuse process involving the whole 
extent of the wall of the stomach. 

Toxic Gastritis. — The mineral acids, the caustic alkalies, arsenic, 
corrosive sublimate, and the metallic salts, phosphorus, camphor, and 
all other irritating materials, cause different lesions of the stomach, ac- 
cording to their quantity, their strength, and the length of time that 
has elapsed before death. 

In large quantities, they destroy and convert into a soft, blackened 
mass both the mucous membrane and the other coats, so that perforation 
may take place. In smaller quantities, they produce black or white 
sloughs of the mucous membrane, surrounded by a zone of intense con- 
gestion. If death does not soon ensue, the ulcerative and cicatricial 
processes which follow such sloughs may contract and deform the 
stomach in various ways. 

If the poisons are of less strength, they produce a diffused congestion 
of the mucous membrane, with catarrhal or croupous exudation on its 
surface, and serous infiltration of the submucous coat (see chapter on 
Poisons). 

ULCERS OF THE STOMACH. 

The Chronic Perforating Ulcer. — This form of ulcer is often seen; 
according to Brinton, in five per cent of persons dying from all causes. 

1 Leube, "Ziemssen's Cyclopaedia," vii., p. 157. 

2 Traus. Lond. Path. Soc, 1875, p. 81. 

3 Trans. Lond. Path. Soc, 1883, p. 90. 



324 



THE ALIMENTARY CANAL. 



It occurs in females nearly twice as frequently as in males. As regards 
the age, Brinton concludes that the liability of an individual to become 
the subject of gastric ulcer gradually rises, from what is nearly a zero at 
the age of ten, to a high rate, which it maintains through the period of 
middle life; at the end of which period it again ascends, to reach its 
maximum at the extreme age of ninety. Lebert gives one hundred and 
ninety-eight cases in which the ulcers were found at the autopsy, as 
follows: 



AGE. 


NUMBER OF CASES. 


AGE. 


NUMBER OF CASES. 


15 to 20 years 

20 to 30 years 

30 to 40 years 

40 to 50 years 


20 

48 
28 
43 


50 to 60 years 


29 


60 to 70 years 


19 


70 to 80 years 


5 











Hauser 1 gives thirty autopsies from Erlangen of ulcers which were 
still open, as follows: 



AGE. 



20 to 30 years. 
30 to 40 years. 
40 to 50 years. 



NUMBER OF CASES. 



AGE. 



50 to 60 years. 
60* to 70 years. 
70 to 80 years. 



NUMBER OF CASES. 



Moore 2 gives -the following table of the fatal cases of ulcer of the 
stomach occurring at St. Bartholomew's Hospital from 1867-1879: 



SEX. 


AGE. 


POSITION. 


CAUSE OF DEATH. 




M. 
M. 
M. 
M. 

M. 


36 
19 

47 
47 
41 
52 
46 
47 
57 
19 
40 
46 


Near pylorus . . 

Greater curve near pylorus 

Near pylorus 

Pylorus 


Perforation. 
Haemorrhage. 
Exhaustion. 
Phthisis. 

Exhaustion. 

Perforation. 

Sinus in liver to lung. 

Haemorrhage. 

Perforation. 




M. 


<■<■ 




M. 
F. 


Lesser curve near pylorus 




M. 


Cardiac end 




M. 


Near pylorus 




F. 


Posterior wall 











Goodhardt 3 describes an ulcer of the stomach, which proved fatal, from 
haemorrhage in an infant at birth. 

The situation of these ulcers, according to Brinton, is as follows: 
In 43 per cent, the posterior surface; in 27, the lesser curvature; in 16, 
the pyloric extremity; in 6, both the anterior and posterior surface; in 5, 

1 Das chron. Magengesch., 1883. 

2 Trans. Lond. Path. Soc, 1880, p. 110. 

3 Trans. Lond. Path. Soc, 1881, p. 79. 



THE ALIMENTARY CANAL, 325 

the anterior surface only; in 2, the greater curvature; in 2, the cardiac 
pouch. Thus about 86 ulcers in ever}' 100 occupy the posterior surface, 
the lesser curvature, and the pyloric sac. 

A.s regards the number of ulcers, two or more are present in about 
twenty-one per cent; there may be two, three, four, or even five ulcers. 
In cases of multiple ulcers, the ulcers are often developed successively. 

In size, the ulcers vary from one-quarter of an inch to five or six 
inches. 

They are usually of circular shape, sometimes oval: sometimes two or 
more are fused together. 

The perforation is largest in the mucous membrane. It may remain 
confined to this, or extend outward and involve the connective tissue, 
muscular and peritoneal coats, its diameter becoming smaller as it ad- 
vances. The ulcer looks like a clean hole punched out of the wall of the 
stomach. Its floor shows no active inflammatory changes. Its edges 
may be in the same condition, or they may be thickened by the growth 
of connective tissue and cells. The rest of the mucous membrane of 
the stomach is apt to be in a condition of chronic catarrhal inflam- 
mation. 

The ulcer may perforate directly through the wall of the stomach, 
and the contents of the latter are discharged into the peritoneal cavity; 
or adhesions are formed between the wall of the stomach and the neigh- 
boring viscera, so that the bottom of the ulcer is closed; or, if the liver, 
the intestines, or the abdominal wall become adherent, they may be in- 
vaded by the ulcerative process, and cavities or fistulse are formed com- 
municating with the stomach; or, if the adhesions are incomplete, a 
local peritonitis and collections of pus may be developed. 

During the progress of the ulcer, there may be repeated small haemor- 
rhages from the erosion of small blood-vessels, or large haemorrhages 
from the erosion of large arteries. 

In many cases these ulcers cicatrize, and such a cicatrization may 
produce various deformities of the stomach. 

It is very difficult to understand how these ulcers are produced. It 
seems probable that the nutrition of a circumscribed part of the wall of 
the stomach is interfered with, and that this portion is then destroyed 
by the action of the gastric juice. But we are still ignorant of the way 
in which the obliteration of the arteries is effected. It has, indeed, been 
demonstrated in animals that an artificial embolism of the branches of 
the gastric arteries will produce ulcers of the stomach; and in the human 
stomach we occasionally meet with cases of embolism of the branches of 
the gastric artery and ulcers. But the clinical history of most cases of 
ulcer of the stomach will not correspond with such a method of causa- 
tion. A chronic obliterating endarteritis would seem to be a more 
probable cause. 



326 THE ALIMENTARY CANAL. 

Hemorrhagic Erosions occur as rounded spots or narrow streaks, 
formed by a loss of substance of the mucous membrane. The mucous 
membrane at these points is congested, soft, and covered by small blood- 
clots. The destruction of the mucous membrane is usually superficial, 
but may involve its entire thickness. The number of these erosions may 
be so great that the entire internal surface of the stomach is studded 
with them. They give rise to repeated haemorrhages, and are accom- 
panied by catarrhal inflammation of the rest of the mucous membrane. 

They occur at all periods of life, even in infants. Their usual seat 
is the pyloric portion of the stomach. 

They may be idiopathic. Usually, however, they occur in connection 
with some serious general disease. 

Follicular Ulcers somewhat resembling the ulcers of the small intes- 
tine are occasionally met with. They are produced by changes in the 
aggregations of lymphatic tissue, which are situated about the blind ends 
of the gastric tubules. 

DILATATION. 

Very considerable degrees of dilatation of the stomach are found at 
autopsies, without stenosis of the pylorus or any other mechanical cause 
to account for them. It is usually difficult to determine how long these 
dilatations have existed and how much effect they have in causing death. 
Nine such cases are recorded by Goodhardt. 1 

Acute Dilatation of the stomach, with vomiting of very large quanti- 
ties of thin fluid, has been observed in a few cases. 2 It is a very curious 
condition, the dilatation of the stomach being developed suddenly and 
without discoverable cause. 

Of the mechanical causes which produce dilatation of the stomach, 
stenosis of the pylorus is the most common. Such a stenosis may be ef- 
fected by a tumor, by chronic inflammation and thickening, and by the 
cicatrization of ulcers. Less frequently obstructions of the small and 
large intestines act in the same way. 

Some forms of chronic gastritis are attended with dilatation of the 
stomach without stenosis. 

In rare cases, circumscribed, sacculated dilatations are produced by 
the presence of foreign bodies— portions of wood, metal, etc. 

TUMORS. 

Papilloma. — It has already been mentioned that in some cases of 
chronic gastritis there are small, polypoid hypertrophies of the mucous 

1 Trans. Lond. Path. Soc, 1883, p. 88. 

2 Trans. Lond. Path. Soc, vol. iv. and vol. xxxiv., p. 82. Hughes Bennett, " Prac- 
tice of Medicine." Fagge, Guy's Hospital Reports, vol. xviii., p. 1. Andral, Clinique 
Medicale. 






THE ALIMENTARY CANAL. 327 

membrane. Besides these, we find polypoid tumors which may reach a 
considerable size. They are composed of a connective-tissue stroma ar- 
ranged' so as to form tufts covered with cylindrical epithelium. In some 
cases, there are also tubules lined with cylindrical epithelium, so that the 
tumor has partly the structure of an adenoma. Fibromata of small size 
are sometimes found in the connective-tissue coat. Lipomata are formed 
in the submucous connective tissue in the shape of rounded or polypoid 
tumors. They usually project inward, but sometimes outward beneath 
the peritoneum. They may also appear in the form of numerous yellow 
nodules beneath the mucous membrane. 

Myomata occur in the form of rounded tumors which originate in the 
muscular coat, but may gradually separate themselves from it and project 
inward or outward. The submucous myomata are at first small tumors 
lying loosely attached in the submucous tissue. As they grow larger 
they push the mucous membrane inward and take the shape of polypoid 
tumors. Lymphomata in the wall of the stomach are seen in some cases 
of leukaemia. 

Sarcomata are said to occur in the wall of the stomach in rare in- 
stances. It must be admitted that in some of the tumors of the wall of 
the stomach, which are ordinarily called cancerous, the structure is not 
well defined, and it is possible that some of them are sarcomata. 

A myo-sarcoma growing outward from the greater curvature of the 
stomach is described by Brodowski. 1 The tumor weighed twelve pounds. 
It was composed largely of smooth muscle cells. There was a secondary 
tumor in the liver. 

Adenoma. — It has been already mentioned that in some of the papil- 
lary tumors of the mucous membrane there is a considerable growth of 
tubules lined with cylindrical epithelium. 

Besides these, we find in the submucous coat circumscribed tumors 
composed of tubules like those of the gastric mucous membrane. 

Small tumors resembling the pancreas have also been seen in the sub- 
mucous and subserous coats. 

Carcinoma of the stomach is almost always primary. But very few 
secondary cases have been recorded. 2 

Primary carcinoma of the stomach is of the colloid variety, or 
common cancer, or cancer with cylindrical epithelial cells, or it is pig- 
mented. 

Colloid cancer is composed of a connective-tissue stroma, arranged so 
as to form cavities of different sizes, which contain colloid matter and 
polygonal cells. It infiltrates first the submucous connective tissue and 
then extends inward and outward. In this way there is formed a 

1 Virch. Arch., Bd. 67, p. 227. 

2 Virch. Arck., Bd. 38 and 86, p. 159. Trans. Path. Soc, London, 1876, p. 264. 



328 THE ALIMENTARY CANAL. 

diffuse thickening of the pyloric end of the stomach rather than a cir- 
cumscribed tumor. Sometimes the whole of the wall of the stomach is 
changed in this way. Secondary tumors are usually situated in the 
peritoneum. 

Carcinoma with cylindrical epithelial cells. These tumors are formed 
of a connective-tissue stroma,, which may contain numerous round cells, 
and of tubules lined with cylindrical epithelium like that of the mucous 
membrane of the stomach. In these tumors, the new growth seems to 
begin in the gastric tubules. As the arrangement of the tubules is more 
or less regular, these tumors maybe called adenomata or carcinomata 
(see Fig. 69), 

Common cancer is formed of a connective-tissue stroma inclosing 
rounded and tubular spaces filled with small, polygonal nucleated cells. 
In some cases this structure is well marked; in others, the stroma is 
abundant and filled with round cells, the spaces are very small, and the 
epithelial cells few. It may then be difficult to distinguish between in- 
flammatory thickening, sarcoma, and carcinoma. 

Both these forms of carcinoma, common cancer and cancer with 
cylindrical cells, run the same course as regards their gross appearance, 
their situation, and their development of metastatic tumors. 

About sixty per cent of these tumors are situated at the pyloric end 
of the stomach, on the lesser curvature or on the posterior wall. The 
cardiac end of the stomach, the greater curvature, or nearly the entire 
wall of the stomach may also be the seats of the new growth, but not as 
frequently. 

The new growth usually follows one or other of three types : 

1. There is a circumscribed, flat tumor formed in the deeper layers 
of the mucous membrane and pushing this membrane inward. After a 
time, the mucous membrane over the centre of the tumor dies, the de- 
structive process involves the tumor also, and so an ulcer with thickened 
edges is formed. In some cases the new growth extends laterally and 
outward, while the central destruction still continues; then the ulcers 
reach a large size, their walls and floor are thick, and peritoneal adhe- 
sions are formed over them. In other cases the ulcer perforates com- 
pletely through the wall of the stomach, unless the opening is closed by 
adhesions to the neighboring viscera. 

2. Large rounded tumors are formed, often several inches in dia- 
meter, which project into the cavity of the stomach. 

3. There is a diffuse, flat infiltration of the deep layers of the mu- 
cous coat, of the connective-tissue coat, and sometimes of the muscular 
coat, which does not ulcerate and hardly forms a tumor. This infiltra- 
tion may be confined to the pyloric end of the stomach, or may involve 
nearly the whole of its wall. 



THE ALIMENTARY CANAL. 329 

There is in most of the cases a good deal of chronic catarrhal inflam- 
mation of the mucous membrane. 

If the pylorus is obstructed, the stomach is often dilated. 

The new growth may extend from the stomach to the oesophagus, but 
it very seldom involves the duodenum. 

Metastatic tumors are very common. The liver, the lymphatic glands, 
and the peritoneum are the parts most frequently affected, but such 
metastases have been seen in nearly every part of the body. 

DEGENERATIONS. 

Calcification of the mucous membrane of the stomach sometimes 
occurs as a metastatic process in connection with extensive diseases of 
the bones. 

Waxy Degeneration sometimes involves the blood-vessels of the mucous 
membrane. 



THE INTESTINES. 
MALFORMATIONS. 

Diverticula of the intestines occur in several different ways: 

1. The abdominal wails are cleft asunder at the navel. The ileum 
opens through this cleft by a narrow aperture in its wall. The lower 
portions of the ileum and the colon are small or entirely closed. 

2. There is an opening in the abdominal wall as before, but there is 
not a direct opening into the ileum. There is a long diverticulum of 
the ileum, with an open end projecting into the opening in the abdomi- 
nal wall. 

3. The abdominal wall is closed. There is a diverticulum of the 
ileum connected with the navel by a solid cord. 

4. There is an unattached diverticulum of the intestine. This is 
much the most common form. The diverticula occur only in the lower 
part of the ileum. They usually spring from the convex surface of the 
intestine, more rarely from its attached border. In the latter case, they 
are joined to the mesentery by a fold of peritoneum. The diverticulum 
forms a pouch, one to six inches long, of about the same diameter as the 
intestine, smallest at its free extremity. 

Such diverticula do not interfere with the functions of the intestines. 
They sometimes form part of a hernia. Sometimes the remains of these 
intestinal diverticula — called Meckel's diverticula — form soft, projecting 
tumors at the umbilicus in children. Microscopical examination of such 
tumors often shows the structure of the intestinal mucosa and muscu- 
laris. If they remain attached by a fibrous cord to the navel, this cord 
may be the cause of incarceration of a portion of the intestines. 
26 



330 THE ALIMENTARY CANAL. 

Cloacae consist in the union of the rectum, bladder, and organs of 
generation in a common outlet. 

1. Simple Cloacce are: (a) Complete, and consist in the common 
opening of the urethra or ureters, the vagina, and the rectum into the 
closed bladder, or into a sinus opening outward, which represents either 
the vagina or the rectum, (b) Incomplete. The rectum opens into the 
vagina, the bladder, or the urethra, while the lower part of the rectum 
is closed or absent. 

2. Cloacce combined with Cleft Bladder. — (a) The simple cleavage 
of ■ the intestines is combined with cleft bladder. The anterior ab- 
dominal wall from the umbilicus to the symphysis, the symphysis, and 
the anterior wall of the bladder are absent; the gap is filled with a 
membrane which represents the posterior wall of the bladder. On to this 
membrane open the ileum, ureters, and vagina, (b) The intestine is 
perfectly formed, but the rectum opens into a common sinus with the 
ureters and vagina; or the ureters open into the cleft bladder, and the 
rectum and external genitals are united; or the ureters open into the 
rectum, and the latter terminates normally. 

3. Cloacce combined ivith Abdominal Hernia. — There is a hernial sac 
containing all the abdominal viscera. At the lower end of the sac is an 
opening leading into a sinus in which open the lower end of the ileum, 
the bladder or urethra, and the ureters. The rectum is absent. 

Atresia Ani consists in a deficient development of the colon or rec- 
.tum. The entire colon may be absent; the rectum may be absent, or 
represented by a solid cord; or the upper or lower part of the colon may 
be absent, or separated by a solid cord. 

More rarely, blind terminations of the small intestines are found, and 
sometimes a narrowing so complete as to close the canal. 

The intestines are also found abnormally shortened in various de- 
grees. 

INCARCERATION. 

1. The most common form is that in which a portion of intestine is 
strangulated by a fibrous band. Such fibrous bands are produced by 
peritonitis, or are remains of foetal growth. They pass from the intes- 
tines to the abdominal wall, or from one part of the intestines to another. 
The intestine becomes in some way caught under one of these bands, 
and is compressed by it. The stricture thus produced may cause a 
gradual accumulation of fasces in the intestine above it, and may last 
for a long time before death ensues. In other cases, the stricture inter- 
feres at once with the circulation of the blood; the intestine is intensely 
congested, becomes gangrenous, and death takes place with the symp- 
toms of general peritonitis. 

2. A portion of intestine becomes caught in some abnormal open- 



THE ALIMENTARY CANAL. 331 

ing in the mesentery or omentum, or in the foramen of Winslow, or be- 
tween the two layers of the mesentery. We have seen a case in which 
twelve feet of intestine had passed through a small opening in the 
mesentery. 

3. A coil of intestine makes half a turn at its base, so that the two 
sides of the loops cross at its base. In this way, the lumen of the intes- 
tine is completely closed, and the vessels are compressed, so that con- 
gestion, peritonitis, and gangrene result. This form of incarceration 
is most frequent in the ascending colon. In the small intestine, it only 
occurs when the gut is fixed by old adhesions. 

4. A portion of the intestine, with its mesentery, makes one or more 
complete turns on itself, closing the canal and compressing the vessels. 

5. A portion of the intestine makes a half or entire turn about its 
long axis. This is very rare, and only occurs in the colon. 

6. The mesentery of a part of the intestine is long and loose, in con- 
sequence of a dragging down of the intestine by a hernia or by habitual 
constipation. The portion of intestine thus permitted to hang down is 
habitually filled with faeces, and by its pressure on some other part of the 
intestine produces an ncomplete stricture. 

INTUSSUSCEPTION. 

This change of position consists in the invagination of one portion of 
intestine in another portion. Usually this takes place in the direction 
of the peristaltic movements, from above downward; more rarely in the 
opposite direction. 

The parts are found in the following condition: There are three por- 
tions of intestine, one within the other. The inner portion is continuous 
with the intestines above the intussusception; its peritoneal coat faces 
outward. The outer portion is continuous with the intestine below; its 
peritoneal coat also faces outward. The inner portion is turned inside 
out, its mucous membrane is in contact with the mucous membrane of 
the outer portion. In rare cases, the intussusception is complioated by 
the invagination of a second portion of intestine in the inner tnbe, and 
even by a third intussusception into the second one. These changes oc- 
cur both in the large and small intestine; most frequently the lower part 
of the ileum is invaginated in the colon. The invaginated portion may 
be from a few inches to several feet in length. The lesion is most fre- 
quently found in early childhood. 

The intussusception, by the dragging and folding of the mesentery 
which it produces, causes an intense congestion of the parts, and even 
large haemorrhages between the coats of the intestine. The congestion 
may induce fatal peritonitis, or gangrene of the intestine, or chronic in- 
flammation and adhesions, and the patient lives for a considerable time 
with symptoms of stricture. In other cases, the invaginated portion of 



332 THE ALIMENTARY CANAL. 

intestine sloughs, the outer and inner portions become adherent, and the 
patient recovers, with or without some degree of stricture. 

Besides this grave form of intussusception, we often find, especially in 
children, one or more small invaginations not attended with congestion 
or inflammation. These are formed during the death agony, or imme- 
diately after death. 

TRANSPOSITION. 

The position of the intestines may be the opposite to that which is 
usually found. The transposition may affect all the abdominal viscera, 
or only a single viscus is transposed. 

WOUNDS — RUPTURES. 

Penetrating wounds of the intestine usually prove rapidly fatal, either 
from shock or from peritonitis. Sometimes, however, the wound be- 
comes closed by the formation of adhesions with the' neighboring parts. 
Sometimes the wound in the intestines becomes adherent at the posi- 
tion of the wound in the abdominal wall, and an intestinal fistula is 
formed. 

Rupture of the small intestine is not infrequently produced by 
severe blows on the anterior abdominal wall. It is noticeable that such 
blows may not produce any marks or ecchymoses of the skin. Such 
ruptures usually prove fatal very soon, but sometimes the patient lives 
several days, and the edges of the rupture undergo inflammatory 
changes. 

Strictures of the intestine are sometimes followed by rupture of the 
dilated intestine at some point above the stricture. 

THE SMALL INTESTINE. 
INFLAMMATION. 

Acute Catarrhal Inflammation of the greater part of the small intes- 
tine is developed as part of the lesion of cholera morbus, and after the 
ingestion of irritant poisons. 

Acute inflammation of the duodenum accompanies gastritis, and 
occurs as an idiopathic condition. 

Acute inflammation of the ileum occurs as an idiopathic condition, 
and accompanies inflammation of the colon and of the solitary and 
agminated glands. 

In many of these cases we infer the existence of the inflammation 
from the clinical symptoms. 

After death, the most marked lesions are the increased production of 
mucus and the congestion. In very severe cases, the inflammation may 
extend to the peritoneal coat. 



THE ALIMENTARY CANAL. 333 

Chronic Catarrhal Inflammation of the small intestine accompanies 
heart disease, phthisis, emphysema, cirrhosis of the liver, and Bright's 
disease. The intestine is coated with an increased amount of mucus; it 
is often congested; there may be a general thickening of all its coats. 

Croupous Inflammation is produced by irritant poisons; it is associ- 
ated with crou])ous colitis, and it occurs as an idiopathic disease. The 
mucous membrane is coated with fibrin, its stroma is infiltrated with 
fibrin and pus, and this infiltration extends to the connective tissue, 
muscular and peritoneal coats. 

Suppurative Inflammation of the submucous connective-tissue coat is 
said to occur in rare cases. It is usually metastatic. It takes the form 
of purulent foci of variable extent, which perforate either inward or 
outward. 

THE SOLITARY AND AGMINATED GLANDS. 

It is not uncommon to find in healthy adults who have died from 
accidental causes a considerable swelling of the solitary and agminated 
glands (lymph nodules) of the ileum, without any reason which we can 
discover to account for this swelling. 

Extensive burns of the skin may be followed by a very marked swell- 
ing of the solitary and agminated glands. 

In persons who have died from the infectious diseases, it is not 
uncommon to find these glands swollen. 

In children, swelling of these glands, often followed by softening and 
the formation of ulcers, accompanies many of the catarrhal inflamma- 
tions of the large and- small intestines. 

In pulmonary phthisis, we very frequently find changes in the solitary 
and agminated glands of the small intestine, less frequently in the soli- 
tary glands of the colou. The changes seem to be of the same character 
as those which take place in tubercular inflammation of lymphatic 
glands in other parts of the body. 

The glands become swollen, their elements are multiplied, tubercle 
granula are formed, the central portions of the glands become cheesy. 
The cheesy degeneration extends; it is followed by softening and by death 
of the mucous membrane over the glands; the softened tissue is discharged 
into the intestine, and ulcers are formed with overhanging edges. After 
this, the ulcer shows no tendency to heal, but, on the contrary, becomes 
larger, usually extending laterally so as sometimes to nearly encircle the 
gut. After death, we find, in different patients, these ulcers in all their 
stages of development. They vary much as to the proportion between 
the tubercular and the ordinary inflammatory changes. In some the 
tubercle granula are numerous, in others they are few or even absent 
altogether. The tubercle bacilli are very constantly found in them. 
There is also usually a tubercular inflammation of the peritoneum over 



334: THE ALIMENT A EY CANAL. 

the ulcers, and sometimes of the lymphatics and glands of the mesentery. 
Although these ulcers often reach a large size, it is but very seldom that 
they perforate into the peritoneal cavity. 

Ulcers of the Duodenum. — A few cases have been recorded in which 
extensive burns of the skin have been followed within a few days by the 
formation of deep ulcers of the duodenum. It is still uncertain how 
these ulcers are produced. 

Chronic perforating ulcers, resembling the chronic ulcers of the 
stomach, are found in the duodenum. They are associated with similar 
ulcers in the stomach or occur by themselves. 

Some curious ulcers of the upper part of the small intestine are 
described by Israel. 1 There were five ulcers, from two and one-half to 
ten centimetres long, encircling the intestine, with irregular, granulating 
surfaces. 

Syphilitic ulcers produced by changes in the solitary and agminated 
glands of the small intestine are sometimes found in infants. 

EMBOLI. 

Emboli have been found in the superior mesenteric artery in a number 
of cases ; in the inferior meseuteric artery they are less frequent. They 
produce an intense venous cougestion of the entire wall of the intestine, 
with haemorrhage into its cavity and its wall. 

THE LARGE INTESTINE. 
INFLAMMATION. 

The mucous membrane of the large intestine is very frequently the 
seat of acute and chronic inflammatory processes. The larger number 
of these belong to the condition which is described clinically under the 
name of dysentery. The inflammation affects most frequently the rectum, 
sometimes the entire length of the colon, sometimes only the upper part 
of the colon. 

Acute Catarrhal Colitis. — -The mucous membrane is swollen and con- 
gested, there is an increased production of mucus, there may be a large 
transudation of serum, there may be some bleeding from the capillary 
vessels. The epithelium desquamates, and the connective tissue and 
glandular coats are infiltrated with a moderate number of pus cells. 

There are curious cases of catarrhal colitis occurring in old and feeble 
persons which are very fatal. After death, we find the mucous mem- 
brane soft and black, and the entire wall of the gut soft and easily torn. 
The intestine looks almost gangrenous, but yet does not seem really to 

1 Charite-Annalen, 1884, p. 707. 



THE ALIMENTARY CANAL. 335 

be so. What the real nature of these cases is I do not know, although 
I have seen several of them. 

Chronic Catarrhal Colitis may succeed acute colitis, or it may begin 
as a chronic affection. Either a portion or the entire length of the colon 
may be involved, and the lesion is found developed in different degrees 
in different cases. The glandular coat is thickened by the growth of 
connective tissue between the tubules, or the tubules may become 
atrophied and the glandular coat is then thin. There may be a com- 
plete destruction of the glandular coat at different points, so that ulcers 
of different sizes are formed. The solitary follicles in the wall of the in- 
testine may be inflamed and softened, and in this way also small round 
ulcers are formed. The connective-tissue coat is thickened; this thicken- 
ing is uniform, or it is more marked at some places than others, so that 
little polypoid tumors are formed, which project into the cavity of the 
colou. The muscular and peritoneal coats are also thickened. 

Croupous Colitis. — This form of inflammation may involve the rec- 
tum alone, or the entire length of the colon, or only its upper portion. 
The mucous membrane is congested and swollen, and coated with a 
layer of false membrane; the connective tissue between and beneath the 
glandular tubules is infiltrated with fibrin and pus, and in severe cases 
the inflammation involves the muscular and peritoneal coats also. The 
inflammation is usually more intense at some places than at others, so 
that the surface of the mucous membrane shows the false membrane in 
isolated patches. Less frequently there is a uniform coating with the 
false membrane. In mild cases, as the inflammation subsides, the pro- 
ducts of inflammation are absorbed, and the wall of the intestine returns 
to its normal condition. In more severe cases, the quantity of the 
inflammatory products is so great that portions of the wall of the intes- 
tine become necrotic. This necrosis may involve only the glandular 
coat, or it may extend deeper into the wall of the intestine. The necrosed 
tissue after a time sloughs away, leaving behind ulcers of different sizes 
and depths. After this the ulcers may cicatrize, or their floors and 
walls may remain in the condition of granulation tissue for an indefinite 
length of time. When the latter is the case, there is added a chronic 
inflammation of the wall of the intestine between the ulcers, with 
changes in the mucous membrane and thickening of the connective 
tissue and muscular coats. 

Small multiple diverticula are not infrequently found along the free 
border of the large intestine, which may be empty or contain faecal 
matter. They appear to be formed, as are the multiple diverticula of the 
bladder (see Bladder), by the crowding of pockets of the mucous mem- 
brane through between the fibres of the muscularis. They appear to be 
usually of no special pathological significance, but they may become the 
seat of inflammation. 



336 THE ALIMENTARY CANAL. 

The Solitary Follicles. — In children, the lymphatic glands (lymph nod- 
nles) in the wall of the large intestine frequently become swollen, soften, 
and form ulcers in cases of catarrhal colitis. In adults, such changes are 
not common except in the dysentery of armies. In army dysentery, the 
changes in the solitary follicles often form the principal part of the 
lesion, although catarrhal or croupous inflammations are usually asso- 
ciated with them. The intestine is thickly studded with small, round 
ulcers originating in the destructive changes in the solitary follicles. 
But these ulcers show a disposition to increase in size and to remain as 
chronic ulcers for a long time. 

The Ccecum. — Catarrhal inflammation of the caecum is not uncom- 
mon. It is usually produced by an habitual accumulation of fasces in 
this part of the intestine. The course of the inflammation is chronic, but 
marked by acute exacerbations. At first the mucous membrane under- 
goes the ordinary changes of chronic catarrhal inflammation; then there 
is a slow suppurative inflammation which extends through the wall of 
the intestine, and produces ulcers and perforations. Through these 
perforations the faeces may pass into the peritoneal cavity, or the per- 
forations are partly closed by adhesions, and abscesses are formed, or 
sinuses into the surrounding soft parts. 

The Rectum. — Besides the inflammatory changes already described as 
existing in the colon, we sometimes find a suppurative inflammation of 
the connective tissue which surrounds the rectum, either associated with 
lesions of the mucous membrane or occurring by itself. 

In adults, the lower end of the rectum is the part of the intestine 
which is the most frequent seat of syphilitic ulceration. Most of these 
ulcers seem to be the result of unnatural coitus, or of infection from 
specific sores of the vulva; but some of them seem to be due to the soft- 
ening of gummy tumors. 

The Vermiform Appendix. — The most frequent form of inflamma- 
tion of the appendix is a suppurative one. The appendix is swollen and 
congested; its walls are infiltrated with pus; at some points there may 
be necrosis and sloughing of portions of its wall. Within the cavity of 
the appendix we find faecal concretions, or foreign bodies, or nothing. 
Such an inflammation may terminate in resolution, but more frequently 
it sets up an inflammation of the surrounding tissues. This inflamma- 
tion may be either a local or general peritonitis, or a suppurative inflam- 
mation of the soft parts about the appendix. 

Less frequently there is a chronic inflammation of the mucous mem- 
brane of the appendix, followed by constriction of its upper portion, 
while the lower part is dilated into a cyst filled with mucus and serum. 
Tubercular inflammation of the appendix is of occasional occurrence. 



THE ALIMENTARY CANAL. 337 

TUMORS. 

Myoma. — Tumors composed of smooth muscle and connective tissue 
grow in the muscular coat and project inward. They may be large 
enough to obstruct the intestine, and may then give rise to intussuscep- 
tion. In the duodenum, such tumors may obstruct the common bile 
duct. Less frequently, these tumors project outward into the perito- 
neal cavity. 

Lipomata may be developed from the submucous coat and grow 
inward, or from the subserous coat and project outward into the peri- 
toneal cavity. 

Polypoid Tumors, projecting into the cavity of the intestine and 
composed of connective tissue and covered with epithelium, are frequently 
found. They are associated with catarrhal inflammation or occur by 
themselves. They are found throughout the intestinal tract, and may be 
single or multiple. They grow from the submucous coat, and project 
inward. Some of them are small, solid, connective-tissue tumors, cov- 
ered by the mucous membrane which they have pushed inward. Others 
are of the same character, but of large size. In others, the connective 
tissue is arranged in branching tufts, covered with cylindrical epithe- 
lium, and in these last tumors there may also be tubules lined with cylin- 
drical epithelium, giving to the growth the characters of an adenoma. 

Adenomata are found in the duodenum and colon. They form flat 
infiltrations of the wall of the intestine, or project inward as polypoid 
tumors. They are composed of tubular follicles, like those of the intes- 
tinal mucous membrane, and of a connective-tissue stroma. In some of 
these tumors the tubules have a tolerably regular shape and arrange- 
ment; there is no infiltration of surrounding tissue; the tumor is of 
benign nature. In other tumors, the tubules are irregular in shape 
and arrangement, and the growth infiltrates the surrounding parts. 
There is no sharp dividing line between these tumors and the carcinomata. 

Carcinomata are found in the colon and the duodenum, and are of 
three varieties. 

1. The new growth is composed of tubules lined with cylindrical epi- 
thelium. It begins as a flat infiltration of the submucous coat, which 
soon surrounds the intestine, infiltrates the whole thickness of the wall 
of the gut, and may extend to the surrounding soft parts. Fungous 
masses project into the cavity of the intestine, while at the same time 
ulcerative and destructive processes are going on. According to the ex- 
act arrangement of the growth, there is more or less stenosis of the in- 
testine. 

2. The growth has the characters of colloid cancer, and forms a dif- 
fuse infiltration of the intestinal wall, completely surrounding it and 
often extending over a length of several inches. 



338 THE ALIMENTARY CANAL. 

3. At the anus there is sometimes a carcinomatous growth, with flat 
epithelial cells (epithelioma), like similar growths in the skin, which in- 
volves the lower end of the rectum. 

Lymphoma. — Tumors composed of tissue resembling that of the 
lymphatic glands originate in the solitary and agminated follicles and in 
the intestinal wall in cases of leukaemia and pseudo-leukaemia. 

Similar tumors are found as an idiopathic lesion both in the large 
and small intestines. These tumors are irregular diffuse growths in- 
filtrating the wall of the intestine, the mesentery, and the neighboring 
glands, and reaching a considerable size. They often ulcerate internally 
and produce dilatation or stenosis of the intestine. It is hard to tell 
whether some of these tumors should be called lymphomata or sarco- 
mata. 

CONCRETIONS. 

There are sometimes found in the intestines round, oval, or irregular 
masses of firm consistence. They are usually small, but may reach the 
size of a man's fist. They are composed of faecal matter, mucus, bile, 
the carbonate and phosphate of lime, and triple phosphate. They may 
produce inflammation, ulceration, and perforation. 

PARASITES. 

Mycosis intestinalis. — Under this name have been described a 
number of cases in which inflammation of the intestines occurred as 
one of a group of lesions. 1 In these cases, there are found ecchymoses 
of the skin and mucous membranes; patches of fibrin in the stomach, 
small intestine, and colon; serum in the peritoneal cavity; swelling of 
the spleen and lymphatic glands; and sometimes inflammation of the 
lungs. The intestinal lesions are most marked in the small intestine 
and the upper part of the colon. The mucous membrane is studded 
with small brownish patches. At the centres of these patches, the wall 
of the intestine is infiltrated with pus, and around the centres it is infil- 
trated with blood. Bacilli resembling those of anthrax are found in the 
intestinal lesions and in other parts of the body. It is believed that the 
disease is a form of anthrax. 

Ascaris lumbricoides is found in the small intestine, either singly or 
in considerable numbers. In rare cases, a number of worms may form 
a mass which produces inflammation, ulceration, and perforation. 

Oxyuris vermicularis is found in large numbers in the rectum. 

Tricocephalus dispar is found in the caecum. 

Ankylostomum duodenale is found in the duodenum, and may give 
rise to considerable haemorrhages. 

1 Virch. Arch., Bd. xxi., p. 579; xxx., p. 366; lii., p. 541. Zeitsch. f. Biologie, 
v., 129. Arch. d. Heilkundc, xv. Arch. f. klin. Med., xii., p. 517. 



THE ALIMENTARY CANAL. 339 

Trichina spiralis is found in its adult condition in the small in- 
testine. 

P ent astomam denticulatum occurs in the submucous tissue of the 
small intestine in an incapsulated condition. 

Cysticercus cellulosw has been seen, in a few cases, on the mucous 
membrane. 

Tcenia solium, Tmnia mediocanellata, and Bothriocephalic s latus are 
all found in the small intestine. 

Very large numbers of various forms of bacteria are regularly found 
in the intestinal cavity intermingled with its contents and clinging to 
its walls. 

THE PERITONEUM. 

The free surface of the parietal peritoneum is covered with a single 
layer of flat, polygonal nucleated cells. Beneath these cells are succes- 
sive planes of connective tissue extending down to the muscles and fas- 
ciae. These planes are formed of a fibrillated basement substance, re- 
inforced by elastic fibres, and of branching cells. Imbedded in the 
connective tissue are the nerves, blood-vessels, and lymphatics. The 
lymphatic system is very extensive. 

The omentum consists of fibrillated connective tissue arranged so as 
to form a meshwork. The trabecules of the meshwork are completely 
covered by large, fiat cells. In the basement substance, beneath the 
endothelium, are branching cells. In the larger trabecular are blood- 
vessels, lymphatics, and fat. Sometimes we find on the larger trabecular 
little nodules formed of polygonal or branched cells. 

MALFORMATIONS. 

Arrest of development of the peritoneum occurs in the shape of fis- 
sures in the mesial line or external to it; in the case of the diaphragm 
being absent, of a fusion with the pleura; and as defective development 
of the mesentery, the omentum, and the other folds of the peritoneum. 

Excess of development occurs in the shape of unusual length of the 
mesentery, the omentum, and the other folds of the peritoneum; or of 
supernumerary folds and pouches. These are chiefly found in the hypo- 
gastric, iliac, and inguinal regions and near the fundus of the bladder. 
There is access to these sacs by a well-defined fissure or ring, which is 
frequently surrounded by a tendinous band lying in the duplicative. 
They may give rise to internal incarceration of the intestines. 

INFLAMMATION. 

The very great extent of the peritoneum, and the readiness with 
which its lymphatic system absorbs foreign matters from the peritoneal 



340 THE ALIMENTARY CANAL. 

cavity, render peritonitis a most severe and dangerous form of inflamma- 
tion. 

If the greater part of the peritoneum is inflamed, we call the lesion a 
general peritonitis. If only a circumscribed area is involved, it is a local 
peritonitis. The course of the inflammation may be rapid or slow, so 
that we speak of acute and chronic inflammation. The inflammation 
may be attended with the production of tubercle tissue, and then it is a 
tubercular peritonitis. 

I. Acute Peritonitis. 

The acute inflammations of the peritoneum may occur as idiopathic 
lesions without discoverable cause; but much more frequently they are 
directly due to some appreciable cause. 

Wounds and contusions of the wall of the abdomen; wounds, ulcers, 
new growths, incarcerations, intussusceptions, ruptures, perforations, 
and inflammations of the stomach and intestines; inflammation of the 
vermiform appendix; injuries, ruptures, and inflammations of the 
uterus, ovaries, and Fallopian tubes; rupture and inflammation of the 
bladder; inflammation of and about the kidneys; abscesses and hydatid 
cysts of the liver; inflammation of the gall bladder and large bile 
ducts; thrombosis of the portal vein; inflammations of the spleen, pan- 
creas, lymphatic glands, retroperitoneal connective tissue, vertebrae, 
ribs, and pelvic bones; septicaemia and the infectious diseases, and 
chronic Bright's disease — are all ordinary causes of acute peritonitis. 

According to the exact cause of the inflammation, the peritonitis is at 
first either local or general. A local peritonitis may remain circum- 
scribed, or it may spread and become general. 

We can distinguish two anatomical forms of acute peritonitis. 

1. Cellular Peritonitis. — This form of peritonitis may be produced 
by any irritant which does not act too energetically. It can be excited 
in dogs by injections of very small quantities of a solution of chloride of 
zinc. In the human subject we find it with perityphlitis, with circum- 
scribed abscesses in the peritoneal cavity,and in cases of puerperal fever 
which die within forty-eight hours after the development of symptoms. 

After death we find the entire peritoneum of a bright-red color, 
from the congestion of the blood-vessels; but there are no fibrin, no 
serum, no pus, no other lesions visible to the naked eye. Minute exam- 
ination, however, shows a very marked change in the endothelial cells. 
They are increased in size and number, and the new cells coat the sur- 
face of the peritoneum and project outward in little masses (Fig. 
156). 

2. Exudative Peritonitis. — The ordinary form of acute peritonitis 
is attended with the production of serum, fibrin, and pus, and with 
changes in the endothelium and connective-tissue cells. 






THE ALIMENTARY CANAL. 341 

If we inject a solution of chloride of zinc or of some other irritant 
into the peritoneal cavity of a dog, we find that by the end of one or two 
hours inflammatory changes are evident. There is a little serum in the 
peritoneal cavity, a general congestion of the peritoneum, and little 
knobs and threads of fibrin on its surface. There are no marked 
changes in the endothelium or connective-tissue cells, but pus cells are 
present in moderate numbers in the stroma, just beneath the endothe- 
lium, and white blood-cells in the vessels. 

After the lapse of twenty-four hours, the lesions are more marked. 







Fig. 156.— Acute Cellular Peritonitis— Human omentum, x 750 and reduced. 

The congestion of the peritoneum is much more decided, there is more 
serum in its cavity and a thicker layer of fibrin and pus on its surface. 
Minute examination shows that two distinct sets of changes are going 
on at the same time: (1) a production of fibrin, serum, and pus; (2) a 
swelling and multiplication of the endothelial cells. If the inflamma- 
tion is very intense, the pus and fibrin are most abundant; if the inflam- 
mation is milder, the changes in the endothelium are more marked. 
The fibrin coagulates on the free surface of the peritoneum. The white 
blood-cells collect in large numbers in the blood-vessels, and as pus cells 
infiltrate the stroma and collect on its surface. There is no special 



342 



THE ALIMENTARY CANAL. 



change in the connective-tissue cells. The endothelial cells may remain 
in place, although their edges and corners are separated by pus cells and 
knobs of fibrin; or the endothelium falls off in large patches; or the 
surface of the peritoneum is covered with numerous cells which look like 
endothelial cells more or less deformed. But few dogs survive the third 
day of an acute artificial peritonitis. 

In the human subject, if death takes place before the third day, both 
the gross and minute changes are the same as those seen in the dog. 
There are present the same general congestion, the pus, fibrin, and 



^f: 




% 




Fig. 15? 



Acute Exudative Peritonitis of eight days 1 duration— Human omentum, x 850 and 
reduced. 



serum, the desquamation and multiplication of the endothelial cells 
(Pig. 157). 

In many cases of peritonitis, however, death occurs between the sixth 
and fourteenth days of the disease. The appearance of the peritoneum 
at this period of the inflammation is not always the same. The conges- 
tion of the blood-vessels may persist, it may be very intense and accom- 
panied with extravasations of blood, or it may be entirely absent. There 
may be a thin coating of fibrin and pus gluing together neighboring sur- 
faces of peritoneum, or this layer may be very thick. The accumulation 
of pus may be superficial, or it may infiltrate the whole thickness of the 
peritoneum and the subperitoneal connective tissue. The quantity of 



THE ALIMENTARY CANAL. 



313 



purulent serum in the peritoneal cavity may be small or large, and this 
serum may contain few or many pus cells, or the serum may be of a dirty 
brown color and filled with bacteria. When the purulent serum is shut 
in by adhesion, it is often thick and yellow, like the pus of an abscess. 

The minute appearances differ from those seen at an earlier stage, 
chiefly in the larger amount of inflammatory products, and in the changes 
in the fixed connective-tissue cells. During the first three days of an 
acute peritonitis, the connective-tissue cells are but little changed, but 
by the seventh day there is a marked increase in their size and number. 

Acute peritonitis may prove fatal by the fourteenth day; or it may 
be succeeded by chronic peritonitis; or the patients recover and perma- 



I : ;; ■ j, ; 





Mf^:- : - WM> 



Fig. 158.— Chronic Cellular Peritonitis occurring with pulmonary phthisis— Human omen- 
tum, x 750 and reduced. 

nent connective-tissue adhesions and thickenings of the peritoneum are 
left behind. Recovery is most common w r hen the peritonitis has been a 
local one. 



II. Chronic Peritonitis. 

We find the following varieties of chronic peritonitis: 
1. Cellular Peritonitis. — This form of peritonitis is found as a com- 
plication of chronic endocarditis, of cirrhosis of the liver, of chronic 
pulmonary phthisis, and of acute general tuberculosis. 

Neither fibrin ntr pus is present, but there may be clear serum in 



344 



THE ALIMENT AKY CANAL. 



the peritoneal cavity. The peritoneum may look normal to the naked 
eye, or it may be studded with very minute, translucent nodules. 

Minute examination shows changes in the endothelial cells and the 
connective-tissue cells. These cells are everywhere increased in number 
and altered in shape; or, to speak more guardedly, the surface of the 
peritoneum is covered with cells which look as if they were derived from 
the endothelium and the connective-tissue cells (Fig. 159). Some are 
large, flat cells; some smaller, polygonal cells; some irregularly fusiform; 
some large, granular masses containing a number of nuclei. Although 




i '.;■■ '-' ' ■. , : j^»«Mfc 



Fia. 159.— Chronic Peritonitis with Adhesions, x 750 and reduced. 
Parietal peritoneum. 



these new cells are found over most of the surface of the peritoneum, 
yet they are more numerous in little patches which are scattered here 
and there. 

2. Peritonitis with Adhesions. — There may be a formation of per- 
manent adhesions without the production of fibrin or pus. It is often, 
indeed, difficult to tell whether old peritoneal adhesions are due to the 
form of chronic peritonitis of which we are now speaking, or whether 
they are the result of an acute peritonitis. But there are some cases 
in which the mode of development of the adhesions seems evident. 



THE ALIMENTARY CANAL. d45 

If, from perityphlitis or some other cause, a collection of pus is shut 
in in some part of the peritoneal cavity, we may find the rest of the 
peritoneum smooth and shining; no serum, fibrin, or pus, no thickening; 
but the neighboring surfaces of the peritoneum are attached to each 
other by adhesions. These adhesions are in the shape of threads and 
membranes, often of the most extreme tenuity. They are formed of a 
fibrillated basement substance, the fibrils crossing each other in all 
directions. In the basement substance are cells, some fusiform and 
stellate, but most of them look like large branching cells, of which the 
cell bodies have become fused with the basement substance while the 
nuclei remain. 

Close to these adhesions the peritoneum may appear normal to the 
naked eye, but if it is put in water very fine threads and membranes 
will float upward from its free surface. Minute examination shows that 
the connective-tissue cells are increased in size and number, that the 
endothelial cells are replaced by cells of a great variety of shapes, and 
that the thin little threads and membranes on the surface are formed of 
large branching cells (Fig. 159). 

Such a peritonitis with adhesions appears to be a more advanced 
stage of the cellular peritonitis just described, but the inflammation, 
instead of stopping at the production of cells alone, goes on to the for- 
mation of membranes. 

We sometimes find in the same patient chronic pleurisy with adhe- 
sions and chronic peritonitis with adhesions. 

3. Chronic Peritonitis with Thickeyiing of the Peritoneum. — This 
form of peritonitis occurs quite frequently as an idiopathic lesion. It 
may involve the greater part of the peritoneum or be confined to the 
capsules of the liver and spleen. 

The most marked feature of the lesion is the thickening of the peri- 
toneum — a thickening which may reach as much as an inch. The outer 
portions of the thickened peritoneum are composed of dense connective 
tissue, the inner layers of granulation tissue. The surface of the perito- 
neum is smooth or covered with fibrin. There may also be connective- 
tissue adhesions between different parts of the peritoneum. The perito- 
neal cavity contains clear or purulent serum. 

In some cases the parietal peritoneum is principally involved; in 
others, the peritoneum of the stomach, intestines, liver, and spleen. 
The thickening of the capsule of the liver is attended with a diminution 
in the size of that viscus. 

4. Chronic Peritonitis ivith the Production of Fibrin, Serum, and 
Pus. — This form of peritonitis may follow acute peritonitis, may be 
due to lesions of the abdominal viscera, or may occur without known 
cause. 

The abdominal cavity contains purulent serum, either free or shut 
27 



346 THE ALIMENTARY CANAL. 

in by adhesions. The surface of the peritoneum is coated with fibrin 
and connective-tissue adhesions. The coils of intestine, and all the 
neighboring surfaces of the peritoneum, are matted together partly by 
fibrin, partly by permanent adhesions. 

5. Rcemorrhagic Peritonitis. — This occurs most frequently as a 
local inflammation. It involves the peritoneum behind and around the 
uterus in the female, and that covering the recto-vesical excavation in 
the male. The affected portion of the peritoneum is covered with layers 
of new membrane infiltrated with blood. The membranes are formed 
of connective tissue containing numerous blood-vessels and infiltrated 
with blood. The extravasations of blood may form tumors of consider- 
able size. 

General hemorrhagic peritonitis is described by Friedreich. 1 In two 
cases of ascites, which had been frequently tapped, he found the visceral 
and parietal peritoneum covered with a continuous membrane of a dif- 
fuse yellowish-brown color, mottled with extravasations of blood. The 
membrane was thickest over the anterior abdominal wall. It could be 
separated into a number of layers. These layers were composed of 
blood-vessels, masses of pigment, branching cells, and fibrillated base- 
ment substance. In many places the extravasated blood was coagulated 
in the shape of round, hard, black nodules. The entire new membrane 
could be readily stripped off from the peritoneum. 

6. Tubercular Peritonitis. — This occurs as one of the lesions of 
acute general tuberculosis, with chronic pulmonary phthisis, w T ith 
tubercular inflammation of the genito-urinary tract, and as a local 
inflammation. 

The gross appearance of the lesion varies. 

When tubercular peritonitis occurs as one of the lesions of general 
tuberculosis, there are numerous small miliary tubercles, increase in the 
size and number of the endothelial and connective-tissue cells, and some- 
times a little fibrin. Some of the miliary tubercles are composed of 
tubercle tissue, others of round and polygonal ceils. 

As a complication of tuberculosis of the genito-urinary tract, we find 
the peritoneum studded with miliary tubercles, coated with fibrin, and 
serum is also present in the peritoneal cavity. 

As a complication of chronic phthisis, there are miliary tubercles in 
the peritoneum of the small intestine immediately over tubercular ulcers 
of the mucous membrane. There may also be thickening of the peri- 
toneum and permanent adhesions. 

Local tubercular peritonitis usually follows one of three types: 

(a) Tubercular Ascites. — The peritoneum is thickened; it is studded 
with masses of tubercle tissue in the form of miliary tubercles or of 

1 Virch. Arch., Bd. 58, p. 35. 



THE ALIMENTARY CANAL. 347 

large, flat masses. The omentum may be much thickened. There are 
but few adhesions, but there is a large amount of turbid serum. There 
may be at the same time tubercular pleurisy, or tubercles in the spleen 
or in the lymphatic glands (lymph nodes). 

(b) Tubercular Peritonitis tvith the Production of a large amount of 
Fibrin. — The peritoneum is studded with miliary tubercles. It is coated 
with a thick layer of soft, gelatinous fibrin, which mats together all the 
neighboring peritoneal surfaces, so that the abdominal cavity seems to be 
filled with a large, boggy mass composed of all the viscera adherent to 
each other, and with the interstices between them filled with fibrin. 

(c) Tubercular Peritonitis with Adhesions. — The peritoneum is 
thickened and there are numerous connective-tissue adhesions. All the 
abdominal viscera are firmly matted together, and there may be collec- 
tions of pus shut in by the adhesions. The adherent coils of intestine 
may ulcerate and open into each other. There are miliary tubercles, or 
large, tubercular nodules or plates. 

TUMORS. 

• 

Fibromata are developed from the subperitoneal connective tissue, 
and project inward into the peritoneal cavity. They are found beneath 
the parietal peritoneum and that covering the intestines. Such tumors 
may reach a very considerable size. 

Lipoma. — Circumscribed tumors composed of fat tissue are formed 
beneath the intestinal and parietal peritoneum. These tumors may be- 
come changed into fibrous tissue or calcified. Their pedicles may be- 
come atrophied so that they are left free in the peritoneal cavity. 

When they grow beneath the parietal peritoneum, they may form fat 
hernias. At the umbilicus, in the inguinal canal, along the vas deferens, 
in the crural ring, and in the foramen obturatorium, fatty tumors may 
grow, project outward under the skin like hernias, and, by drawing the 
peritoneum after them into a pouch, may open the way for a future 
intestinal hernia. 

Plexiform Angio- Sarcoma. — Very large tumors, resembling in their 
gross appearance colloid cancer, have been described by Waldeyer. 1 
They are formed Jby a new growth of blood-vessels, with a production of 
gelatinous tissue from their adventitia. 

Carcinoma of the peritoneum is either secondary or primary. The 
primary tumors assume the character of colloid cancer or of common 
cancer. 

The colloid form frequently involves the greater part of the perito- 
neum, and forms a large mass which distends the abdomen. The omen- 
tum is changed into a large, gelatinous mass; the subjacent muscles, the 

1 Virch. Arch., Bd. 55, p. 134. 



348 THE ALIMENTARY CANAL. 

lymphatic glands, and the liver are infiltrated with the new growth, and 
soft, gelatinous masses project into the peritoneal cavity. The umbili- 
cus is sometimes invaded, so as to project outward in the form of a semi- 
translucent tumor. The appearance of the new growth is that of a soft, 
jelly-like mass imbedded in a fibrous stroma. The minute structure is 
that of a connective-tissue stroma, arranged so as to form cavities of 
different sizes. These cavities are filled with a homogeneous, gelatinous 
basement substance and with polygonal cells. 

Common carcinoma appears in the form of numerous small nodules 
scattered everywhere in the inner layers of the peritoneum. These 




Fig. 160.— Section of a Retroperitoneal Sarcoma, x 850 and reduced. 

nodules are small, firm, and white, and are composed of a fibrous stroma 
inclosing cavities filled with polygonal cells. With the formation of 
these nodules there are often associated a general thickening of the peri- 
toneum, an accumulation of serum in the peritoneal cavity, and adhe- 
sions. 

Endotheliomata of the peritoneum have been observed in cases with 
similar growths in the pleura (page 226). 

Sarcomata appear in the form of solitary, slowly growing tumors 
behind the peritoneum or between the folds of the mesentery. 

These retroperitoneal sarcomata are found both in children and. 






THE ALIMENTARY CANAL. 349 

adults. They usually originate behind the peritoneum covering the pos- 
terior part of the abdominal wall. At first they grow slowly inward, 
pushing forward the peritoneum and abdominal viscera. After a time 
they assume a more infectious character, infiltrating the soft parts with 
which they come in contact, and forming metastatic tumors in the liver 
and other viscera. 

These tumors are composed of a stroma and cells. The cells are 
large, of cuboidal shape, and often undergo fatty degeneration, when 
they become swollen. The proportion between the cells and the stroma 
and the arrangement of the cells vary in the different cases and in dif- 
ferent parts of the same tumor (Fig. 160). 

The stroma may be abundant and the cells scattered irregularly, 
each cell in a little cavity of its own. The stroma may be abundant, 
but the cells are collected in masses, as in a carcinoma. 

The cells are abundant and close together, but each cell is surrounded 
by a thin partition of connective tissue. The blood-vessels are numerous, 
and the cells are arranged around them with some regularity. 

From the above description, it will be seen that these tumors are 
of peculiar structure, and perhaps do not really belong to the sarcomata. 

PARASITES. 

Echinococci can be formed in their regular way at any part of thevis- 
.ceral and parietal peritoneum, or be free in the peritoneal cavity. These 
cysts may be small, or so large as nearly to fill the abdominal cavity. 

Cysticercus cellulosce may also be developed in the subperitoneal con- 
nective tissue. 



THE LIVER 



MALFORMATIONS. 



Congenital malformations of the liver are not common, and are of 
little practical importance. The organ may be entirely wanting; the lobes 
may be diminished or increased in number; its form may be altered, so 
that it is rounded, flattened, triangular, or quadrangular. The gall 
bladder or gall ducts may be wanting; the ductus choledochus may be 
double, both ducts emptying into the duodenum, or one emptying into 
the duodenum, the other into the stomach. The single ductus chole- 
dochus may also empty into the stomach. Owing to abnormal openings 
in the diaphragm or the abdominal parietes, the liver may suffer dis- 
placement upward or forward. In congenital transposition of the viscera, 
the liver is found on the left side, the stomach and spleen on the right 
side. 

Small, isolated bodies, having the same structure as the liver, have 
been found in the suspensory ligament. 

ACQUIRED CHANGES IN SIZE AND POSITION. 

As a result of tight lacing, very marked changes are sometimes pro- 
duced in the shape of the liver. By the narrowing of the base of the 
thorax, the organ is compressed from side to side, and its convex surface 
.is pressed against the ribs. In consequence of this there are found 
ridges and furrows on its convex surface. In consequence also of the 
circular constriction, a part of the right, and usually of the left lobe also, 
becomes separated by a depression. Over this depressed and thinned 
portion of the liver the capsule is thick and opaque. In extreme cases, 
the depressing and thinning reach such an extent that there is only a 
loose, ligamentous connection between the separated portion and the 
liver. 

A series of depressions are sometimes found on the upper surface of 
the right lobe of the liver, running from front to back, apparently caused 
by folds of the organ. 

Structural changes in the liver may induce changes in its size and 
shape. It may be increased in size by tumors, hydatid cysts, abscesses, 



THE LIVER. 351 

fatty and amyloid degeneration, by congestion, and sometimes by cirrho- 
sis, etc. 

Tt may be diminished in size by atrophy, by cirrhosis, by acute paren- 
chymatous degeneration, etc. 

Changes in the position of the liver are produced by alterations in 
its size, by pressure downward from the thoracic cavity and upward 
from the abdomen, by the constriction of tight lacing, by tumors or cir- 
cumscribed serous exudation between the liver and diaphragm, by cur- 
vature of the spine. 

The liver is readily turned, by pressure from above or below, on its 
transverse axis. The transverse colon may be fixed above the liver so as 
to push it backward, downward, and to the right. There are a few cases 
recorded of dislocated and movable livers. These occurred in women 
who had borne children and whose abdominal walls were lax. With 
ascites it is not uncommon to find the liver quite movable. 

ANEMIA AND HYPEREMIA. 

Ancemia of the liver may be general or partial. It may be due to 
general anaemia or to local disturbances of the circulation, such as swell- 
ing of the cells in parenchymatous or other degeneration, pressure of 
tumors, etc. The organ appears pale, often of slightly yellowish or 
brownish color. It may be harder than usual, and smaller. 

HypercBmia of the liver is either an active or a passive process. In 
health, the amount of blood in the liver varies at different times, being 
regularly increased during the process of digestion. When the digestive 
process is unduly influenced by the ingestion of spirits, spices, etc., the 
hyperaemia assumes abnormal proportions, and when this is often repeated 
it may lead to structural changes in the organ. Severe contusions over 
the region of the liver sometimes cause a hyperemia, which may result 
in suppurative or in indurative inflammation. In hot climates and in 
malarious districts, active and chronic hyperemia of the liver are fre- 
quent, and often cause structural lesions. In scurvy, also, the liver is 
sometimes congested. Cessation and suppression of the menses and 
haemorrhoidal bleeding may cause hyperaemia of the liver. In all these 
varieties of active congestion, the liver is enlarged, of a deep-red color, 
and blood flows freely from its cut surface. 

The passive congestions of the liver are produced by some obstruction 
to the current of blood in the hepatic veins. Valvular diseases of the 
heart, emphysema and fibrous induration of the lungs, large pleuritic 
effusions, intrathoracic tumors, angular curvature of the spine, aortic 
aneurisms pressing on the vena cava, and constrictions of the vena cava 
and of the hepatic veins, may all produce a chronic hyperaemia of the 
liver. In all these cases, as the congestion affects principally the hepatic 
veins, we find the centre of each acinus congested and red while its 



352 



THE LIVER. 



periphery is lighter colored. This gives to the liver a mottled or nut- 
meg appearance {nutmeg liver). The liver cells in the centre of each 
acinus are frequently colored by little granules of red or black pigment, 
and the cells at the periphery become fatty, so that the nutmeg appear- 
ance is still more pronounced. A liver in this condition is usually of 
medium size, but may be smaller or larger than normal. 

When the congestion is long-continued, the veins at the centre of 
each acinus may become permanently dilated, the hepatic cells in their 
meshes become atrophied (Fig. 161), so that the centre of each acinus 




-.:\;;;*y;*-.-; 










v **:-:-.'..-^.-jV-:5>.- 



85Si 



Fig. 161.— Chronic Congestion of the Liver (Nutmeg liver). 
This section shows complete atrophy of the liver cells at the centre of the lobule, a, dilated 
vena centralis; b, dilated capillaries filled with blood; c, portal vein surrounded by connective tis- 
sue; d, gall duct; e, atrophied liver cells; g, nearly normal liver tissue. 



consists only of dilated capillaries or of these and new connective tissue; 
or the dilatation and atrophy of the liver cells may, in circumscribed 
portions of the organ, involve the entire acinus. In long-continued 
congestion, the liver is usually smaller than normal, and may be slightly 
roughened or uneven on the surface; but it is sometimes enlarged. The 
peculiar nutmeg appearance may be very well marked, or it may not be 
evident, the organ being of a dark-red color. 



THE LIVER. 353 

WOUNDS. RUPTURE, AND HAEMORRHAGE. 

Wounds of the liver may induce haemorrhage, which, if life continue, 
is followed by inflammation. Serious wounds of the liver are usually 
fatal, but recovery may occur even after the destruction of a consider- 
able portion of the organ. 

Rupture of the liver may be produced by severe direct contusions or 
by falls. It may be produced in children by artificial delivery. The 
rupture usually involves both the capsule and a more or less considerable 
portion of the liver tissue. It is commonly accompanied by large haem- 
orrhage, and is usually fatal. 

Haemorrhage. — Extravasations of blood in the substance of the liver, 
or more frequently beneath the capsule, are found in new-born children 
after tedious or forcible labors. In adults, haemorrhage, except as the 
result of injury, is uncommon. Extravasations of blood are sometimes 
seen in malignant malarial fevers, especially in tropical climates; in 
scurvy, purpura, and phosphorus poisoning; and bleeding may occur in 
and about soft tumors, abscesses, and echinococcus cysts. It may also 
occur as a result of thrombosis of the hepatic vein. 

LESIONS OF THE HEPATIC ARTERY. 

The hepatic artery is in rare cases the seat of aneurisms which may 
attain a large size. Such aneurisms may displace the liver tissue, com- 
press the bile ducts so as to cause jaundice, and may rupture into the 
stomach or abdomen. 

Owing to its abundant anastomoses, emboli of the branches of the 
hepatic artery usually induce no marked lesions, but they sometimes re- 
sult in haemorrhagic infarctions. 

LESIONS OF THE PORTAL VEIN. 

Thrombosis, Embolism, and Inflammation. — Thrombosis of the 
branches of the portal vein may be produced by weakening of the circu- 
lation from general debility — marasmatic thrombi ; by pressure on the 
vessel from without, as in cirrhosis, tumors, gall stones, dilatation of the 
bile ducts, etc.; by injury; by the presence of foreign materials within 
the vessel; and as a result of inflammation of its wall, or of embolus. 
The thrombus may form in the vessels in the liver, or be propagated into 
them from without. It may partially or entirely occlude them. The 
clot may become organized as a result of endophlebitis, and a permanent 
occlusion of the vessel ensue. If the clot be a simple, non-irritating one, 
leading to occlusion, the consequences are usually more marked in the 
abdominal viscera than in the liver itself. The branches of the hepatic 
artery form sufficient anastomoses to nourish the liver tissue and prevent 
its necrosis, even in complete occlusion of the portal vein; and if occlu- 
sion occur slowly, the organ may continue to perform its functions. 



354 THE LIVER. 

But this obliterative form of thrombosis is usually attended by ascites, 
enlargement of the spleen, dilatation of the abdominal veins, and some- 
times by haemorrhage from the stomach and intestines. 

In another class of cases, in addition to the local and mechani- 
cal effects of a thrombus, there may be necrotic changes and suppurative 
inflammation in the walls of the vessels, or in the liver tissue about them. 
The thrombi are apt to soften and break down, and the fragments may 
be disseminated through the smaller trunks of the portal vein. In this 
w T ay, by the distribution through the smaller vessels of a disintegrated 
thrombus from a large trunk, or by the introduction into the branches 
of the portal vein of purulent or septic material from some of the ab- 
dominal viscera or from wounds, multiple foci of purulent inflammation 
in the portal vein, and multiple abscesses involving the liver tissue, may 
be produced. In many cases, the presence of bacteria may be detected 
in the inflammatory foci. 

These soft thrombi of the portal vein and the accompanying pyle- 
phlebitis and abscess may be caused in a variety of ways. Ulceration 
of the intestines and stomach, abscesses of the spleen, suppurative in- 
flammation of the mesentery and mesenteric glands, inflammation and 
ulceration of the bile ducts from gall stones, inflammation of the umbili- 
cal vein in infants, may all induce thrombi in their respective veins, 
which maybe propagated to the portal vein or may give rise to purulent 
or septic emboli. Two cases are recorded in which a fish bone in the 
portal vein induced suppurative inflammation in that vessel. One of 
these cases, occurring in Bellevue Hospital in 1867, was reported by Dr. 
Janeway. Male, 47; dying, after a four weeks' illness, in a typhoid con- 
dition, with lesions of sero-fibrinous peritonitis and chronic diffuse ne- 
phritis. There were numerous small abscesses in the right lobe of the 
liver, two in the left lobe. The left division of the portal vein contained 
a firm red and white clot over an inch long; the right division was lined 
with a firm thrombus. The walls of the vein were thickened and con- 
tained purulent fluid. A fish bone, two inches long, its centre covered 
by a thrombus, lay half in the mesenteric and half in the portal vein. 

In certain cases of thrombosis and inflammation of the portal vein, 
the cause cannot be discovered. 

In infants, inflammation of the umbilical vein may not only induce 
inflammation of the portal vein and abscesses in the liver, but multiple 
abscesses in various parts of the body, and acute peritonitis may be in- 
duced. 

Rupture of the Portal Vein, with fatty degeneration of its walls, has 
occurred in a few instances. 

Chronic EndophleMtis, with atheroma and calcification, may occur in 
the walls of the portal vein, giving rise to thrombosis. 

Dilatation of the Portal Vein, either uniform or varicose, may occur 






THE LIVER. 355 

in various parts of the vessel or its branches. It may be caused by de- 
struction of the liver capillaries in cirrhosis, or by occlusion of the vein 
by thrombi, tumors, etc. 

THE HEPATIC VEINS. 

The hepatic veins present lesions similar to those of the portal vein 
and its branches, but they are much less frequent. They may be dilated 
by obstruction to the passage of venous blood into the heart. They may 
be the seat of acute and chronic inflammation, and soft thrombi and 
suppurative inflammation may be produced by abscesses in the liver. 

ATROPHY OF THE LIVER. 

Atrophy of the liver may affect the entire organ or be confined to some 
part of it. General atrophy may occur in old age as a senile change, or 
may be induced by starvation or chronic exhausting diseases. The or- 
gan is diminished in size, is usually firm, and the acini appear smaller 
than usual. Microscopically the change is seen to be due to a diminu- 
tion in size of the liver cells, and hand-in-hand with this there occurs 
frequently an accumulation of pigment granules within the atrophied 
cells. The cells may entirely disappear over circumscribed areas, leav- 
ing only shrivelled blood-vessels and connective tissue; or, in some cases, 
there may be an increase of connective tissue in connection with the 
atrophy of the cells. When much pigment is formed in the cells, the 
lesion is often called pigment atrophy. 

Essentially the same changes may occur in circumscribed portions of 
the liver, as the result of pressure from new connective tissue in cirrho- 
sis, from tumors, hydatids, amyloid degeneration, gall stones, etc. In 
atrophy from pressure, the liver cells are apt to become very much flat- 
tened and squeezed together as they diminish in size. 

DEGENERATIVE CHANGES. 

Parenchymatous Degeneration (Cloudy Swelling). — In a variety of 
acute and infectious diseases — pneumonia, typhoid and typhus fevers, 
scarlatina, variola, diphtheria, erysipelas, yellow fever, septicaemia, and 
in certain cases of acute anaemia and phosphorus poisoning — the liver 
is somewhat swollen and, on section, of a dull yellowish-gray color, 
looking somewhat as if it had been boiled. It contains less blood than 
usual, and the outlines of the lobules are indistinct. Microscopical ex- 
amination shows the lesion to consist of a swelling of the liver cells and 
an accumulation in them of moderately retractile, finer and coarser albu- 
minous granules. Those granules may disappear and the cells return to 
their normal condition, or, as is frequently the case, they may pass into 
a condition of fatty degeneration. Very frequently fatty and parenchy- 
matous degenerations are associated together. 



356 THE LIVEK. 

Fatty Infiltration. — In the normal human liver, there is usually a 
certain amount of fat in the liver cells, and this amount varies consid- 
erably under different conditions. 

The gross appearance of pathological fatty livers varies a good deal, 
depending upon the amount and distribution of fat and its association 
with other changes. If the lesion is uncomplicated and considerable, 
the organ is increased in size, the edges rounded, the consistence firm, 
the color yellowish, and the cut surface greasy. The lobules are en- 
larged and their outlines usually indistinct, and the blood-content 
diminished. The liver is increased in weight. If the amount of infil- 
tration be moderate, the outlines of the lobules may be more distinct 
than usual, and the centres appear unusually red. This is due to the 
fact that the accumulation of fat usually commences in the periphery 
of the lobules and progresses towards the centres, so that the centre 
appears darker by contrast with the fatty periphery. The lesion may be 
uniform throughout the organ or it may occur in patches. In the lat- 







Fig. 162.— Fatty Infiltration of Liver Cells. 

ter case, the liver has a mottled appearance, irregular yellowish patches 
alternating with the brownish -red, unaffected portions. 

Fatty infiltration is often associated with chronic congestion {nutmeg 
liver), with cirrhosis and amyloid degeneration; the picture may then 
present considerable complexity. Fatty livers may be stained brown or 
greenish with bile pigment. 

Microscopically the liver cells are seen to contain larger and smaller 
droplets of fat (Fig. 162), and frequently large drops of fat occupy nearly 
the entire volume of the cell, so that the protoplasm may be visible only 
as a narrow, nucleated crescent at one side, or it may disappear alto- 
gether. The microscopical appearances, of course, vary, depending upon 
the degree of infiltration and the association with other lesions. 

Fatty infiltration of the liver may occur as a result of excessive in- 
gestion of oleaginous food; in chronic alcohol, phosphorus, and arsenic 
poisoning; in certain exhausting diseases accompanied by malnutrition, 
as in pulmonary phthisis, chronic dysentery, etc., and under a variety of 
conditions which we do not understand. 



THE LIVER. 



357 



Fatty Degeneration. — In this condition, which in many cases cannot 
be morphologically distinguished from fatty infiltration, the fat is be- 
lieved to be formed by a transformation of the protoplasm of the liver 
cells. The fat-droplets are, for the most part, very small and abundant, 
though this is not constant. Fatty degeneration of the liver cells fre- 
quently follows, and is associated with, cloudy swelling under the vary- 
ing conditions in which this occurs, or it may appear in profound anae- 
mia and in acute phosphorus and arsenic poisoning. 

Amyloid Degeneration (Waxy Liver). — In the liver, amyloid degene- 
ration may be general or local; so extensive as to give the organ very 
characteristic appearances, or so slight as to be unrecognizable without 
the aid of the microscope. It may be associated with other lesions. 
When the change is extensive and general, the liver is enlarged some- 
times to more than twice its normal size; the edges are thickened and 




Fig. 163.— Amyloid Degeneration of Liver Capillaries. 



rounded; the surface smooth; the tissue tough, firm, inelastic, more or 
less translucent, and of a brownish-yellow color. The lobular structure 
may be more or less indistinct, or it may become very evident by an 
associated fatty degeneration of the peripheral or central cells of the 
lobules. The translucency and peculiar appearance of the tissue may be 
best seen by slicing off a thin section and holding it up to the light. 
When the lesion is less considerable, the liver may be of the usual size, 
and may feel harder than normal, and here and there a translucent 
mottling may be evident, or the degeneration may be apparent only on 
the addition of staining agents (see page 66). When, as is frequently 
the case, it is associated with cirrhosis, the liver may be small and 
nodular, and the appearance of the cut surface will vary greatly, de- 
pending upon the character of the cirrhotic change and the presence or 
absence of fat. 



358 THE LIVER. 

This degeneration usually commences in the walls of the intralobular 
blood-vessels, causing them to become thickened and translucent. The 
liver cells are squeezed by the thickening of the vessels and may become 
partially or completely atrophied (Fig. 163). 

It is stated by some observers that the liver cells may also become 
waxy, but we have been unable to find them unmistakably thus changed. 
The liver cells not infrequently undergo fatty metamorphosis. Amyloid 
degeneration may also involve the interlobular vessels, and in advanced 
stages larger and smaller areas of liver tissue maybe nearly or completely 
converted into the dense, refractile substance which in its arrangement 
but obscurely represents the grouping aud structure of the affected 
lobules. Not infrequently atrophic or fatty liver cells are seen scattered 
singly or in clusters through the amyloid masses. In the affected regions 
the blood-content of the liver is considerably diminished, or it may be 
nearly entirely absent. 

Amyloid degeneration of the liver is usually associated with a similar 
lesion of other organs, such as spleen, kidneys, intestines, etc., although 
it may occur in this organ alone. It usually occurs in cachectic condi- 
tions, as in chronic phthisis; in chronic suppurations, especially of the 
bones; in syphilis, and sometimes in malarial poisoning. It occasionally 
occurs unassociated with any of these conditions. 

PIGMENTATION OF THE LITER. 

As a result of severe malarial poisoning, a variable amount of brown, 
black, or reddish pigment is often found in the blood. This is usually 




«t£*W 



Fig. 164.— Pigmentation of the Liver in Malarial Fever. 
The pigment in this specimen was contained in cells lying within the liver capillaries. 

mostly taken up by the leucocytes and deposited in various parts of the 
body, chiefly in the liver, spleen, and marrow of the bones. In the liver 
it is usually found inclosed in variously shaped cells, which lie especially 
in the blood-vessels, but sometimes in the tissue between them (see Fig. 
164). The liver cells frequently contain bile pigment, but usually are 
free from the melanotic pigment characteristic of this malarial condition. 
As the result of this accumulation of pigment, the liver may have a dark 
reddish-brown, an olive-brown, or black color (sometimes called bronze 



THE LIVER. 359 

liver). This condition may be associated with various other lesions of 
the liver, depending upon the nature and extent of which the organ 
will present a great variety of appearances. Thus there may be fatty 
or waxy degeneration, cirrhosis, chronic congestion, etc. 

Pigment may be found in the connective tissue along the portal ves- 
sels similar in character to that which occurs in the lungs from the inha- 
lation of coal dust. This inhaled pigment, according to the researches 
of Weigert, doubtless finds access to the blood, (see page 60), and is de- 
posited in the liver as it is in the spleen and hepatic lymph nodes. 

Pigmentation of the liver cells, which is to a certain extent normal, 
may be greatly increased as a result of atrophy, localized haemorrhage, 
and of obstructive jaundice. 1 

ACUTE YELLOW ATROPHY OF THE LIVER, 

This disease is characterized anatomically by a rapid diminution in 
the size of the liver as the result of a granular and fatty degeneration 
and disintegration of the liver cells. The liver, sometimes within a few 
days, may be reduced to one-half its normal size. On opening the abdo- 
minal cavity, the organ may be found lying concealed by the diaphragm, 
close against the vertebral column. The amount of diminution and the 
general appearance of the affected organ depend to a considerable extent 
upon its previous condition — i.e., whether or not it was the seat of other 
lesions — as well as upon the degree of degenerative change. In general, 
if the lesion is well marked, the liver is small, flabby — sometimes almost 
fluctuating — and the capsule wrinkled. On section, the cut surface may 
show but little trace of lobular structure, but presents an irregular mot- 
tling with gray, ochre-yellow, or red; sometimes one, sometimes another 
color preponderating. 

Microscopical examination shows varying degrees of degeneration 
and destruction of the liver cells. Most evidently in those parts which 
have a grayish appearance, the outlines of the cells are preserved and the 
protoplasm is filled with larger and smaller granules. In the yellow 
portions, the outlines of the liver cells may be preserved, and they may 
contain varying quantities of larger and. smaller fat-droplets and granules 
of yellow pigment. Or the cells may be completely disintegrated, and 
in their place irregular collections of fat-droplets, pigment granules, red 
and yellow crystals, and detritus; only the connective tissue and blood- 
vessels of the original liver tissue remaining. The red areas may show 
nearly complete absence of liver cells and cell detritus, and sometimes 
irregular rows of cells which are variously interpreted, as being new- 
formed gall ducts or proliferated liver cells. In these areas it appears 

1 The distribution and amount of the pigment may be well seen by staining thin 
sections with eosin and mounting in eosin-glycerin or balsam. 



360 THE LIVER. 

to be, in part at least, the blood contained in the vessels which imparts 
the red color. Sometimes the interstitial tissue is infiltrated with small 
spheroidal cells resembling leucocytes. Crystals of leucin and tyrosin 
are sometimes found intermingled with the cell detritus. In some cases 
the liver is not diminished in size. 

These lesions of the liver are frequently associated with enlargement 
of the spleen and parenchymatous degeneration of the kidney and of the 
heart muscle. Multiple haemorrhages may occur in the gastro-intestinal 
canal, kidneys, bladder, and lungs. There is usually marked jaundice. 
Eod-shaped bacteria and micrococci have been found in the liver, but 
their significance is doubtful; we have not been able to find them in the 
cases which we have examined. The cause of the disease is unknown, 
and it is doubtful whether it is a disease primarily of the liver, or a gen- 
eral disease with local lesions. It is not unlikely that more than one 
form of lesion is grouped under this heading. 

INFLAMMATION" OF THE LIVER. 

Acute Hepatitis (Purulent Hepatitis; Abscess of the Liver). — Puru- 
lent or suppurative inflammation of the liver may be the result of injury; 
it may be secondary to inflammation of the gall ducts or the branches 
of the portal vein. It may occur as the result of the presence of tumors, 
parasites, or from propagation of an inflammatory process from without, 
as in ulcer of the stomach with adhesions to the liver and secondary in- 
volvement of the latter. It is probably directly due to the introduction 
into the organ, through the blood-vessels or otherwise, of bacteria. 
Purulent inflammation in the liver almost always results in abscess. 

Large abscesses of the liver may be traumatic, but are, for the most 
part, due to unknown causes. They are not infrequently associated with 
dysentery, and may then be due to the conveyance through the veins of 
septic material from the intestinal ulcers. They occur most frequently 
in tropical climates, but are not very uncommon in the temperate zones. 
They are usually single, but there may be several of them. They are 
sometimes so large as to occupy a large part of a lobe. They are most 
frequent in the right lobe, but may occur in any part of the organ. 
They tend to enlarge, and as they do so they approach the surface of the 
liver. Here the contents of the abscess may be discharged into the peri- 
toneal cavity. More frequently, however, as they approach the surface, 
a localized adhesive peritonitis ensues, so that the liver becomes bound to 
adjacent parts, and thus the abscess may open into the pleural cavity, 
or, owing to a secondary pleurisy with adhesions, into the lung tissue. 
They may open into the pericardium. They may open externally through 
the abdominal wall; into the stomach, duodenum, colon, or pelvis of the 
right kidney; into the hepatic veins, portal vein, vena cava, or gall blad- 
der or gall ducts. 



THE LIVER. 361 

The early stages in the formation of large abscesses of the liver are 
but little known. It is probable, however, that in many cases they are 
the result of the confluence of smaller abscesses. Their contents, usually 
bad smelling, may be thick and yellow, like ordinary pus; but more com- 
monly they are thin, reddish brown or greenish in color, from admixture 
with the pus of blood, gall pigment, and broken-down liver tissue. Mi- 
croscopical examination shows the contents to consist of fluid with pus 
cells, more or less degenerated blood, degenerated liver cells, fragments 
of blood-vessels, and pigment granules and crystals. The walls of the 
abscess are usually ragged, shreds of necrotic liver tissue hanging from 
the sides. Microscopical examination of the liver tissue near the abscess 
shows infiltration with pus, flattening of the liver cells from pressure, 
cloudy swelling, and necrosis of those lying along the cavity. 

After the discharge of the contents of the abscess, or without this if 
it be not very large, granulation tissue may form in the wall of the cavity, 
and a fibrous capsule be produced, inclosing the contents, which become 
thickened and often calcareous, and in this condition may remain for a 
long time. Or the connective-tissue walls may approach one another 
and join, forming a fibrous cicatrix at the seat of the abscess. 

Abscesses of the liver accompanying inflammation of the portal vein 
and gall ducts are considered elsewhere in this section. 

Small multiple metastatic abscesses are not infrequent in pyaemia, and 
are called pycemic abscesses. In these abscesses we can readily study the 
various stages of formation. Suppurative processes in any part of the 
body — in the head, upper and lower extremities, etc. — may favor the 
production of the noxious materials, which in most cases are probably 
associated with bacteria, or are bacteria themselves. These, entering 
the circulation, may pass the heart and pulmonary capillaries, with or 
without inducing lesions in the lungs, and, lodging in the vessels of the 
liver, induce circumscribed necrosis of the liver tissue and suppurative 
inflammation. Under these conditions, we may find on a section of the 
liver larger and smaller yellowish or grayish spots, the larger of which 
may be soft and present the usual characters of abscesses. The smaller, 
which may not be larger than a pin's head, may present the usual con- 
sistence of liver tissue with the lobular structure still evident, others 
may be softer, more yellow, and surrounded by a zone of hyperaemic 
liver tissue. Microscopical examination of the earlier stages often shows 
the blood-vessels filled with micrococci, scattered and in masses. 
Around these the liver cells are found in various stages of necrosis; in 
many the nuclei do not stain, and the bodies are very granular; or the 
entire cell is broken down into a mass of detritus. About these necrotic 
islets of liver cells pus cells collect and often form a zone of dense infil- 
tration. Thus, by the increase of pus cells and the necrosis of liver 
tissue, small abscesses are formed, whose contents are intermingled with 
28 



362 THE LIVER. 

greater or less quantities of bacteria, which seem to increase in number 
as the process goes on. By the confluence of small abscesses, larger ones 
may be formed. Death usually ensues, however, before the abscesses at- 
tain a very large size. 

Chronic Interstitial Hepatitis (Cirrhosis). — The primary result of 
chronic interstitial hepatitis is the formation of new connective tissue 
in the liver. The character, amount, and distribution of the new tissue 
vary greatly in different cases. Secondarily there are usually marked 












y& 




Fig. 165.— Chronic Interstitial Hepatitis. 
a, new-formed connective tissue; 6, dilated blood-vessels of the new tissue; c, gall duct; 
d, parenchyma of liver. 

changes in the liver cells and in the blood-vessels and gall ducts. The 
new tissue is most commonly formed and most abundant in the peri- 
phery of the lobules along the so called capsule of Grlisson, but it may 
extend into the lobules between the liver cells. It may surround single 
lobules, or more frequently larger and smaller groups of lobules (Fig. 
165). It may occur in broad or narrow, irregular streaks or bands. It is 
frequently more abundant in one part of the liver than in another. The 



THE LIVER. 363 

new-formed tissue tends to contract, and thus compromise by pressure 
the inclosed islets of liver tissue, causing them to project, in larger and 
smaller nodules, from the surface of the organ. The liver cells may be 
flattened or atrophied from pressure; or, from interference with the 
portal circulation, they may atrophy or become fatty; or they may be- 
come colored with bile pigment. The varied appearances which cirrhotic 
livers present to the naked eye depend largely upon the amount and dis- 
tribution of the new connective tissue, and upon the secondary changes 
in the liver cells. 

In some cases the liver is enlarged, sometimes so much so as to weigh 
nine or ten pounds, the surface smooth or slightly roughened; in other 
cases it may be finely or coarsely nodular on the surface. It may be 
smaller than normal, sometimes very small indeed, so as to weigh only 
one or two pounds. The surface may then be very rough and uneven 
from the projection of larger and smaller nodules of liver tissue, or it 
may be quite smooth; or the organ may be greatly distorted by the con- 
traction of large bands or masses of new connective tissue. In section 
through cirrhotic livers, the new tissue may not be visible to the naked 
eye, or it may appear as grayish, irregular streaks, or bands, or patches, 
often sharply outlined against the dark-red, or brown, or yellow, or 
greenish-yellow parenchyma. 

On microscopical examination, the new connective tissue is found 
in some cases loose in texture, and containing many variously shaped 
cells; or it may be dense and contain comparatively few cells; it is 
usually quite vascular. Xot infrequently, when occurring largely be- 
tween the lobules, it will be found to have incroached more or less upon 
their peripheral portions. Very frequently there are found in the new 
connective tissue cylindrical ducts lined with cuboidal cells, and re- 
sembling gall ducts (Fig. 166, c); or irregular rows of more or less cuboidal 
or polyhedral cells, which look somewhat like the lining cells of the 
medium-sized gall ducts, or like altered liver cells. The branches of the 
hepatic and portal veins, particularly the latter, often become obliterated 
by pressure from the new connective tissue, or from chronic thickening 
of their walls, so as to seriously interfere with the function and nutrition 
of the liver cells. The bile ducts also may become obliterated, or there 
may be catarrhal inflammation, especially of the larger trunks. The 
branches of the hepatic artery are much less liable to alterations than 
the other vessels. The capsule of the liver is usually thickened either 
uniformly or in irregular patches; or its surface may be roughened by 
larger and smaller papillary projections. The liver is frequently bound 
to the diaphragm or other adjacent organs by connective-tissue adhe- 
sions. Amyloid and fatty degeneration may be associated with cirrhosis. 
Cirrhotic livers frequently show an unusual number of leucocytes in the 
blood-vessel3. 



364 



THE LIVER. 



The obstruction to the portal circulation induced by cirrhosis usually 
gives rise to a number of secondary lesions, since collateral circulation 
is rarely established in sufficient degree to afford much relief. The 
hemorrhoidal and vesical veins may be greatly enlarged, and also veins 
of communication between Glisson's capsule and the diaphragmatic 
veins. 

In rare cases, a very peculiar dilatation of the cutaneous veins about 
the umbilicus is observed. The enlarged veins form a circular network 
around the umbilicus, or a pyramidal tumor alongside of it, or all the 
veins of the abdominal wall, from the epigastrium to the inguinal region, 
are dilated. This condition is said to be produced by the congenital 




Fig. 166.— Chronic Interstitial Hepatitis. 
Showing a portion of the section shown in Fig. 165, but more highly magnified, a, portions of 
liver lobules; 6, new-formed connective tissue; c, gall ducts, apparently new formed ; d, blood- 
vessels in the new tissue. 



non-closure and subsequent dilatation of the umbilical vein and its anas- 
tomoses with the internal mammary, epigastric, and cutaneous veins. 
According to Sappey, it is not the umbilical vein which is dilated, but a 
vein which accompanies the ligamentum teres. 

There is very frequently also a dilatation of the veins of the abdomi- 
nal wall, which has a different cause. It is produced by the pressure of 
the fluid of ascites on the vena cava, and is found with ascites from any 
cause and with abdominal tumors. 

Ascites is the most common secondary lesion of cirrhosis. It usually 



THE LIVER. 365 

begins at an early stage of the disease, and is apt to increase constantly. 
It usually precedes oedema of the feet, but both may appear at the same 
time. This fluid is of a clear yellow or brown, green or red; it is some- 
times mixed with shrews of fibrin, and more rarely with blood. The 
peritoneum remains normal, or becomes opaque and thick, or there 
may be adhesions between the viscera. 

The spleen is very frequently enlarged, and the enlargement may be 
very considerable. When it is not increased in size, this seems usually 
due to previous atrophy of the organ, or to fibrous thickening of its 
capsule, or to haemorrhages from the stomach and bowels, occurring just 
before death. 

The stomach and intestines are often secondarily affected by the 
obstruction to the portal circulation. Profuse haemorrhage from the 
stomach and intestines may occur, and sometimes cause sudden death. 
The mucous membrane is then found pale, or congested, or with hemor- 
rhagic erosions. Sometimes the blood is infiltrated in the coats of the 
stomach and intestines. The mucous membrane of the stomach, and of 
the entire length of the intestines, is frequently the seat of chronic 
catarrhal inflammation, and is sometimes uniformly and intensely con- 
gested and coated with mucus. In other cases both the mucous and 
muscular coats are pale, but very markedly thickened. 

Cirrhosis of the liver is not infrequently accompanied by chronic 
diffuse nephritis. 

The causes of cirrhosis are imperfectly understood. It is a disease 
of adult life, but exceptionally occurs in children. In adults, it seems 
in many cases to be directly dependent upon the continued ingestion of 
large quantities of strong alcoholic liquors. It very rarely occurs as a 
result of beer drinking. There are many cases of cirrhosis for which no 
cause can be discovered. 

SypMlitic Hepatitis. — Chronic interstitial inflammation of the liver 
very frequently results from syphilitic infection, either congenitally or 
in the later stages of the acquired form. It may occur in a diffuse 
manner, new connective tissue being formed either between the lobules, 
or within them between the rows of liver cells. The. new tissue may be 
rich in cells, or dense and firm. This form is frequently seen in chil- 
dren, and cannot be distinguished, either macroscopically or microscopi- 
cally, from similar forms of interstitial hepatitis from other causes. 

In other cases, particularly in children, there may be numerous small 
gummata (so-called miliary gummata) scattered through the liver, to- 
gether with more or less new connective tissue (Fig. 167). In adults, 
gummata are usually larger, varying in size from that of a pea to a hen's 
egg, and may be surrounded by larger and smaller irregular zones of 
ordinary connective tissue (Fig. 168). In still other cases in adults, we 
find larger and smaller dense, irregular bands or masses of connective 



366 THE LIVER. 

tissue running through the liver, drawing in the capsule, and often 
causing great deformity of the organ. These bands and masses of new 
tissue may or may not inclose gummata, either large or small. These 
deforming cicatrices, either with or without gummata, are very charac- 
teristic of syphilitic inflammation of the liver. 

This, like the simple interstitial inflammation of the liver, may be 
associated with fatty and waxy degeneration, and with atrophy of the 
parenchyma from pressure. 

Tubercular Hepatitis. — This lesion, which is usually secondary to 



■.;.'. \_7n- '': : <0H 






Fig. 167.— Syphilitic Hepatitis. 
A so-called miliary gumma from the liver of a child with congenital syphilis. 

tubercular inflammation in some other part of the body, or a part of 
acute general miliary tuberculosis, is most frequently characterized by 
the formation of larger and smaller miliary tubercles, which may be 
either within or between the liver lobules, or in the walls of the bile 
ducts. Many of the tubercles are too small to be seen with the naked 
eye; others may be just visible as grayish points; still others may be from 
one to three mm. in diameter, with distinct yellowish-white centres. 
Microscopical examination shows considerable variation in the structure 
of the tubercles in different cases, as well as in the same liver. Some of 
them, usually the smaller ones, consist simply of more or less circum- 



THE LIVER. 



367 



scribed collections of small spheroidal cells, which are not morphologi- 
cally distinguishable, so far as the form and arrangement of the cells are 
concerned, from simple inflammatory foci, or from the diffuse masses of 
lymphatic tissue which occur normally in the liver. 

In other forms we find a well-marked reticulum with larger and 
smaller spheroidal and polyhedral cells, with or without giant cells. In 
still other forms there is more or less extensive cheesy degeneration. 
The larger forms are conglomerate, being composed of several tubercle 
granula joined together to form a single nodular mass. The liver cells 
at the seat of the tubercle are destroyed, and the interstitial tissue and 
blood-vessels either destroyed or merged into the tubercle tissue. In 
the periphery of the tubercles the liver cells may be in a condition of 






a. 







' 



- •,'-■■■: /! 



4 ■«£&* 



Fig. 168.— Gumma of Liver. 
a, cheesy centre; b, fibrous periphery; c, small-celled peripheral infiltration; d, portions of 
liver lobules. 

coagulation necrosis, and the tissue round about may be infiltrated with 
small spheroidal cells. There is in some cases a new formation of gall 
ducts or of structures which resemble these, and which in transverse 
sections look considerably like giant cells. Tubercle bacilli, frequently 
in small numbers, but often in great abundance, may be found within 
the tubercles. 

Tuberculosis of the liver may be associated with cirrhosis, waxy and 
fatty degeneration. 

Much more rarely than the above form there are found in the liver 
more or less numerous scattered tubercular masses from the size of a 
pea to that of a walnut or larger, with cheesy centres and usually a new 
growth of connective tissue in the periphery. These so-called solitary 



368 THE LITER. 

tu~bercl.es of the liver may be softened at the centres. Tubercular inflam- 
mation of the gall ducts may give rise to numerous scattered, cheesy 
nodules, as large as a pea or larger, which may be softened at the centre 
and stainel yellow with bile. This lesion is rare and seems to be more 
frequent in children than in adults 

Perihepatitis. — Acute inflammation of the serous covering of the 
liver, with the formation of fibrin, may occur as a part of acute general or 
localized peritonitis, and over the surface of abscesses, tumors, hydatids, 
etc., of the organ, when these lie near or approach the surface; or it may 
be secondary to acute pleurisy. 

Chronic perihepatitis, resulting in the thickening of and formation of 
new connective tissue in and beneath the capsule of the liver, may be 
secondary to an acute inflammation of the capsule, or it may be chronic 
from the beginning and associated with chronic pleurisy, chronic peri- 
tonitis, and cirrhosis. In this way, more or less extensive adhesions of 
the liver to adjacent structures may be formed; or, by contraction of the 
new-formed connective tissue, considerable deformity of the liver may 
be produced. The capsule is sometimes uniformly thickened, sometimes 
the new tissue occurs in more or less sharply circumscribed patches. 
The surface is sometimes roughened from little, irregular projecting^ 
masses of connective tissue. Microscopically the new-formed tissue is 
usually dense and firm, but it may be loose in texture and contain many 
cells. Not infrequently bands or masses of connective tissue run inward 
from the thickened capsule between the superficial lobules, causing local- 
ized atrophy of the parenchyma. 

Hyperplasia of Lymphatic Tissue in the Liver. — In some forms of 
leukaemia and pseudo-leukaemia, the liver is not infrequently enlarged 
and soft and besprinkled with small white spots, or streaked with narrow 
whitish, irregular bands, or of a diffuse grayish color. Microscopical ex- 
amination shows this change to be due to an accumulation of cells. re- 
sembling leucocytes, either along the portal vein, or diffusely through 
the liver tissue, or in small circumscribed masses. The amount of accu- 
mulation of these small cells varies much, but is sometimes so great as to 
seriously compromise the liver cells. The origin of these new cells is not 
yet definitely known. They may be, and doubtless in part are, brought 
to the organ through the portal vein, but they may, in part at least, be 
formed in the liver itself. 

In typhoid fever, small-pox, scarlatina, diphtheria, and measles, 
small circumscribed masses of cells resembling leucocytes are sometimes 
found in the liver, lying in the meshes of a delicate reticular tissue. 
These are sometimes called 'miliary lymphomata; but it should be re- 
membered (see p. 301) that small masses of lymphatic tissue normally oc- 
cur in the liver r and that as, under the above conditions, an hyperplasia 
of the lymph nodes and spleen is wont to occur, these so-called lympho- 



THE LIVER. 369 

mata are very probably normal structures, which have become more 
prominent under the conditions of disease owing to an acute inflamma- 
tory condition induced by absorbed ptomaines. 

TUMORS OF THE LIVER. 

Tumors of the liver may be primary or secondary; the latter are most 
common. 

Cavernous Angiomata. — These tumors, usually small, from five to 
fifteen mm. in diameter, are most common in elderly persons and are of 
no practical significance. They may be situated at the surface or im- 
bedded in the organ, and are of a dark-red color; sometimes sharply cir- 
cumscribed by a conuective-tissue capsule, sometimes merging imper- 
ceptibly into the adjacent liver tissue. Microscopically they consist of a 
congeries of irregular cavities (Fig. 66, page 145), filled with blood and 
frequently communicating freely with one another. The walls of the 
cavities consist of connective tissue, often containing small blood-vessels, 
and are sometimes thick, sometimes thin. They are believed to be 
formed by dilatation of the liver capillaries, with subsequent thickening 
of their walls and atrophy of the adjacent liver cells. 

Small fibromata and lipomatah&ve been described, as alsofibro-neuro- 
mata of the sympathetic. 

Adcyiomata of the liver are of not infrequent occurrence. They are 
sometimes small and circumscribed, sometimes very large and multiple. 
They present two tolerably distinct types of structure. In one form the 
tissue presents essentially the same structure as normal liver tissue,, ex- 
cept that the arrangement of the cells is less uniform and the cells are 
apt to be larger. They look like little islets of liver tissue, sometimes 
incapsulated and sometimes not, lying in the liver parenchyma. In the 
other form, the cells are less like liver cells, are frequently cylindrical, 
and are arranged in the form of irregular masses of tubular structures 
with more or less well defined lumina. These tumors are sometimes 
large and multiple, and in one case described by Greenfield there were 
metastatic tumors in the lungs. These tubular adenomata are in some 
cases so closely similar to some of the carcinomata as to be scarcely dis- 
tinguishable from them, and seem, indeed, to merge into them. 

Carcinomata are the most common and important of the liver tumors, 
and may be primary or secondary. Primary carcinomata of the liver are 
probably developed from the epithelium of the gall ducts, and in some 
cases are arranged along the larger trunks. Their cells are usually poly- 
hedral, sometimes cylindrical, and may be arranged irregularly in alveoli 
or form more or less well-defined tubular structures. 

Secondary carcinomata of the liver, which are by far the most com- 
mon, are most frequently due to the dissemination in the organ of tumor 
cells from carcinomata of the stomach, intestines, pancreas, or gall blad- 



370 THE LIVER. 

der. But they may be the result of metastases from the mamma, oeso- 
phagus, uterus, and various other parts of the body. In secondary car- 
cinomata, the cells resemble more or less closely the type of those forming 
the primary tumor. 

The form in which the carcinomatous nodules in the liver present 
themselves is subject to considerable variation. Sometimes they are 
single, but more often multiple; they may be very large, or so small as 
to be scarcely visible to the naked eye; very frequently numerous small 
nodules are grouped in the periphery of a larger cancerous mass. They 
are sometimes deeply imbedded in the liver, sometimes they project 
from the surface. The liver is frequently enlarged, sometimes enor- 
mously so. The nodules are usually whitish, or yellowish, or pink in 
color, but they are often the seat of haemorrhages, and may become soft- 
ened at the centre, forming cysts filled with degenerated tumor tissue 
which is often mixed with blood. The nodules are sometimes hard, 
sometimes soft and almost diffluent. Fatty degeneration is frequent, 
and may be evident to the naked eye in the form of yellowish streaks or 
patches on the cut surfaces. Owing to the degeneration and partial 
absorption of the central portions of the tumors, the nodules on the 
surface frequently present a shallow depression at the centre The 
tumors may be sharply outlined against the adjacent liver tissue, or may 
merge imperceptibly into it. They may be so large or numerous as to 
occupy the greater part of the enlarged organ. The liver tissue in their 
vicinity shows flattening and atrophy of the liver cells from pressure, 
and there may be infiltration with small spheroidal cells. The tumors 
may press upon the portal vein or its branches, or upon the gall ducts, 
and thus seriously interfere with the functions of the organ. Sometimes, 
however, the tumors are very large and abundant without causing any 
apparent detriment to the liver functions. They are not infrequently 
stained with bile. Melanotic carcinomata sometimes occur in the liver, 
most frequently as secondary tumors. 

In some cases, instead of forming separate, distinct nodules, the can- 
cerous growth develops in the form of a diffuse infiltration of the organ, 
so that the often greatly enlarged liver is irregularly mottled with white 
and reddish-brown masses, and may then somewhat resemble some forms 
of chronic interstitial hepatitis. 

Sarcomata. — Spindle-celled, melanotic, and telangiectatic sarcomata 
may occur in the liver as secondary tumors. Secondary myxomata and 
chondromata have also been described, but they are very rare. 

Cavernous lymphangiomata have been described in a few cases. 
Cysts, usually of small size, may occur by dilatation of the bile ducts. 
They may be multiple and contain serum, mucus, and degenerated 
epithelium. Single cysts, apparently unconnected with the gall ducts, 



THE LIVER. 



371 



are occasionally found in the connective tissue of the liver. They may 
be lined with ciliated epithelium. 

The liver is sometimes the seat of larger and smaller multiple cysts, 
varying from microscopical size up to that of a pea, and sometimes 
larger. They do not appear to communicate with the gall ducts. They 
are sometimes associated with multiple cysts of the kidney. Their 
origin and nature are not understood. 1 

Occasionally the liver is found at the autopsy, even if this be made but 
a few hours after death, more or less completely riddled with small, irreg- 
ular-shaped cavities, from the size of a pin's head to that of a pea. 
These holes appear to be due to the accumulation of putrefactive gases 
in the liver, and close about them, as well as in the blood-vessels, large 
bacilli and other forms of bacteria may be found. 2 

PARASITES. 

Echinococcus. — This parasite is the most common and important of 
those which occur in the human liver. It forms the so-called hydatids 
of the liver. These represent one of the developmental stages of the 
small tape-worm of the dog, Taenia echinococcus (see page 73). The 
cysts in the liver may be very small and multiple, but they may be as 
large as a man's head or larger. The liver may be greatly increased in 
size, and the tissue about the cysts atrophied. The liver itself furnishes 
a .connective-tissue capsule, within which is the translucent, lamellated 
membrane furnished by the parasite. On the inside of this we may find 
a layer of cells, granular matter, and a vascular and muscular system 
belonging to the parasite. Projecting from this inner capsule are the 
brood capsules and heads or scolices of the immature tape-worm. The 
scolices may become detached from the wall and lie free in the cavity, 
which is filled with a transparent or turbid fluid. Not infrequently the 
cysts are sterile, and are then simply filled with clear or turbid fluid; or 
the embryos may have died and disintegrated, and their detritus, includ- 
ing the hooklets, may be intermingled with the fluid contents of the 
cysts. The contents of the cysts may be mixed with fat, cholestearin 
crystals, pus, bile, or blood; or form a grumous mass, in which we may 
or may not be able to find the hooklets of the scolices or fragments of 
the lamellated wall. The connective tissue of the walls of the cysts may 
be greatly thickened or they may be calcified. 

In other countries the lesion is much more common and frequently 
more formidable than in the United States. The cysts reach an enor- 
mous size, the veins of the liver may be compressed and filled with thrombi, 

1 Consult Pye-Smith, " Cystic Disease of Liver and both Kidneys." Trans. Lon- 
don Path. Soc, vol. xxxii., p. 112, 1881. 

2 Freeman, Trans. New York Path. Society, 1889. 



372 



THE LIVER. 



the bile ducts compressed and ulcerated. So much of the liver tissue 
may be replaced by the hydatids that the patient may die from this 
cause alone. Very frequently there is local peritonitis, and adhesions 
are formed between the liver and the surrounding parts. In some cases 
the cysts rupture, and their contents are emptied into the peritoneal 
cavity, the stomach, the intestines, the pleural cavity, or the lung tissue. 
Sometimes the cysts perforate the bile ducts, the vena cava, or some of 
the branches of the portal or hepatic veins. Sometimes the abdominal 
wall is perforated and a fistula formed between the cavity in the liver 
and the surface. 

In cases in which we do not find the scolices entire, a careful exami- 
nation of the inner cyst wall or of its contents will frequently establish 




Fig. 169.— Echinococcus multilocularis of the Liver. 



the diagnosis by revealing single hooklets (see Fig. 13, page 75) or 
fragments of the characteristically lamellated wall (see Fig. 11, page 74). 
Echinococcus multilocularis, which is apparently an abortive form of 
the above species (see page 75), is very rare indeed in the United States. 
The writer (T. M. P.) has examined a specimen sent to him by Dr. 
Edward J. Ill, of Newark, N. J., and which is now in the museum of 
the College of Physicians and Surgeons, New York. The patient was 
a male, age thirty-one, German, single, farmer. He had been in the 
United States five years. For a year previous to his death he had been 
out of health, and jaundiced, and somewhat emaciated. A large, indis- 
tinctly fluctuating tumor was evident in the right lumbar and umbilical 



THE LIVER. 373 

regions, and apparently connected with the liver. Aspiration of the 
tumor gave a milky fluid believed to be pus. An opening was made into 
the tumor by one of the surgeons attending the case, and death occurred, 
after ten hours, from haemorrhage. 

The liver was found adherent to the abdominal walls, and about one- 
fourth of the right lobe of the liver was occupied by an irregular cavity 
with very rough, ragged walls. These walls were in some places from 
one to two inches in thickness, and appeared to the naked eye to consist 
of dense connective tissue in irregular bands and fascicles, which inclosed 
very irregular, mostly small cavities. Microscopical examination showed 
that the cavities were lined with the delicate, lamellated cuticula charac- 
teristic of the echinococcus cysts. ISTo hooklets were found. Eig. 169 
is a drawing from this specimen. 

Distoma hepaticum, D. sinense, D. lanceolatum, may occur in the 
gall ducts and gall bladder. D. sinense occurs especially in the East, 
and has been found in great numbers in the bodies of Chinamen. D. 
haematobium is very common in Egypt and Abyssinia, occurring in the 
blood-vessels of the liver. 

Pentastoma denticulatum is the undeveloped form of Pentastoma 
taanioides, a parasite which inhabits the nasal cavity of dogs and some 
other animals. In the liver of man, it usually occurs in the form of 
small rounded, calcified cysts. The cysts may contain fat, calcareous 
matter, and the remains of the dead parasite, among which the hooklets 
may be found. 

Ascaris lumbricoides sometimes finds its way from the intestines into 
the bile ducts. It may cause no disturbance here, but in some cases the 
worms have been present in large numbers, and caused occlusion, dilata- 
tion, and ulceration of the biliary passages, and have led to the forma- 
tion of abscess of the liver. 

Psorospermim, the very common parasite in the rabbit's liver, has 
been found a few times in the liver of man. 

THE BILIAEY PASSAGES. 

Catarrhal Inflammation most frequently attacks the lower portion of 
the common duct and the gall bladder. In the acute form, it usually 
leaves but few changes appreciable after death. An abnormal coating 
of mucus, and sometimes congestion of the blood-vessels, are almost the 
only post-mortem lesions. Owing to the swelling of the mucous mem- 
brane and the accumulation of mucus in the lumen, the ducts may be 
temporarily occluded; but this occlusion may not be evident after death. 
If, however, the inflammation becomes chronic, the walls of the bile 
ducts may become thickened and their lumina more or less permanently 
obstructed. In consequence of this, dilatation or ulceration of the bile 
ducts may ensue. Temporary obstruction of the bile ducts may produce 



374: THE LIVEE. 

marked pigmentation of the liver, owing to the accumulation of pigment 
granules in the liver cells, particularly in the vicinity of the capsule of 
Glisson, and jaundice of the entire body. 

The gall bladder may be inflamed by itself or in connection with in- 
flammation of the biliary passages. If the disease is chronic, the wall 
of the bladder maybe thickened; polypoid growths may occur in the 
mucosa; the duct may be occluded; dilatation, ulceration, the formation 
of gall stones, calcification, and atrophy may ensue. 

Inflammation of the stomach and duodenum, hyperemia and inflam- 
mation of the liver, concretions, and parasites, are the usual causes of 
catarrhal inflammation of the biliary passages, but it may occur without 
these. 

Suppurative and Croupous Inflammation may attack the biliary pas- 
sages and produce infiltration of pus in their walls and purulent fluid in 
their cavities; or flakes and tubular casts of fibrin on their walls; or in- 
filtration of their walls with fibrin, and consequent ulceration. These 
lesions occur most frequently in connection with obstruction of the bile 
ducts, and in typhoid and typhus fever, pyaemia, cholera, or they may 
be due to the extension of inflammatory processes from without. They 
also occur under unknown conditions. Suppurative inflammation may 
produce perforations of the ducts or bladder, with escape of bile and peri- 
tonitis; or fistulous openings between the gall bladder and the duodenum, 
colon, and stomach, or through the abdominal wall. Or the inflamma- 
tion may extend to the liver tissue and produce abscesses. Under the 
latter conditions, we may find a series of small abscesses ranged along 
the walls of the suppurating gall ducts. In more advanced stages, the 
abscesses may become large and communicate with one another, so that 
a considerable portion of the liver may be occupied by a series of com- 
municating cavities with ragged walls, containing pus and detritus of 
liver tissue more or less tinged with bile. 

These abscesses are apt to contain various forms of bacteria, but 
whether they always or frequently stand in a causative relation to the 
lesion or not has not been definitely established. 

Such abscesses may become more or less completely inclosed by con- 
nective-tissue walls. The portal vein may also become inflamed, and 
perforations may be formed between it and the bile ducts. 

Constrictions of the biliary passages may also be produced by the same 
causes. 

Constriction and Occlusion may be produced by inflammation of the 
ducts themselves, by new growths in their walls, by calculi or parasites 
in their lumina, by changes in the hepatic tissue in chronic and acute 
hepatitis, by aneurisms, or by pressure on the duct from without, as by 
tumors in the head of the pancreas, etc. 

The obliteration of the smaller bile ducts produces no marked lesions. 






THE LIVEK. 375 

When the ductus communis, or the hepatic duct, is obstructed, the ducts 
throughout the liver are frequently dilated and the liver tissue bile- 
stained. The liver may undergo atrophy and the whole body be intensely 
jaundiced. When the cystic duct is obstructed, the gall bladder is di- 
lated. 

Dilatation of the bile ducts is usually produced by strictures in the 
ways just mentioned, or by calculi. When calculi have produced the 
dilatation, this condition may sometimes continue after they have found 
their way into the intestines. Sometimes, however, we meet with very 
marked dilatation of the bile ducts without being able to make out any 
present or past obstruction. The dilatation may affect only the common 
and hepatic ducts, or it may extend to the smaller ducts in the liver, 
which are then dilated uniformly or sacculated. They may contain 
bile, mucus, or calculi. The liver is at first enlarged, but may afterward 
atrophy. The gall bladder may be dilated in consequence of obstruction 
of the common or the cystic duct. In the latter case, it may reach an 
immense size and form a large tumor in the abdominal cavity. The 
dilatation is generally uniform, the bladder retaining its normal shape; 
sometimes, however, there are diverticula, which are usually produced 
by calculi. If the obstruction to the hepatic duct is incomplete or mova- 
ble, the gall bladder may contain bile, and often calculi. If the obstruc- 
tion is complete, the contained fluid may gradually lose its biliary char- 
acter, and become a serous or mucous fluid of a light yellow color — 
hydrops cystidis fellce. The walls of the bladder maybe of normal 
thickness, or thinned, or thickened, or calcified. If the obstruction is 
due to a calculus, this may pass into the intestine and the gall bladder 
be suddenly emptied. Usually the bladder fills again, owing to its loss 
of contractile power. 

Biliary Calculi. — These bodies are of common occurrence. They 
are found usually in the gall bladder, sometimes in the hepatic, cystic, 
and common ducts; less frequently in the small ducts of the liver. In 
the gall bladder from 1 to 7,800 calculi have been counted. They vary 
in size from that of a pin's head to that of a hen's egg, or they may be 
larger. Single gall stones are usually spheroidal or ovoidal; when mul- 
tiple, they are usually flattened at the sides or faceted. 

They may be composed : 

1. Principally of cholestearin, and may be of pure white color, or 
tinged with various shades of yellow or brown by bile pigment. The 
fractured surface shows a radiating crystalline structure. 

2. Of cholestearin, bile pigment, and salts of calcium and magnesium. 
These are usually dark-colored, brown, reddish-black, or green, and may 
be spheroidal or faceted, smooth or rough on the surface; the fractured 
surface is usually radiating crystalline. This is the most common fornix 



376 THE LIVEK. 

3. Principally of bile pigment. Such calculi are rare, usually small, 
very dark-colored, and not numerous. 

4. Of calcium carbonate. These are rare, have a nodular surface, and 
a clear crystalline, not radiating fracture. 

Most calculi are formed around a central mass, sometimes called the 
nucleus, which may consist of cholestearin, bile pigment, mucus, or epi- 
thelium, or more rarely of some foreign body. Thus a dead parasite, a 
needle, and fruit seeds may serve as nuclei. The body of the calculus 
may be homogeneous, or lamellated, or crystalline. 



'.•'-•"»'.■<. '•'■'■-. : .-: :'■.'.■•■}.'■,£•'■: •:;•..,-.."";*•'.' ■'. -' -"--'- ■•-■"'-■ .'-~."- .'/.'•-' .'-'.-- ^W 

Fig. 170. — Primary Carcinoma of the Common Bile Duct, x 300 and reduced. 

Biliary calculi in the gall bladder may produce no symptoms and only 
be discovered after death. In the hepatic and common ducts they may 
obstruct the flow of bile and produce fatal jaundice; or they may pass 
from time to time into the intestine, producing biliary colic. If they are 
impacted in the cystic duct, they may produce dilatation of the gall blad- 
der. They may get into the duodenum by ulceration through the walls 
of the ducts or gall bladder, or in the same way into the peritoneal cav- 
ity. Gall stones which get into the intestinal cavity usually pass off 
without doing any further injury, but very large calculi may cause occlu- 
sion of the gut, with fatal results. 



THE LIVER. 377 

TUMORS OF THE GALL BLADDER AXD LARGER GALL DUCTS. 

Small fibromata have been described in the gall bladder and in the 
common duct, but they are very rare. The most common tumors are 
carcinomata. These may be primary or secondary, and present the usual 
structural variations. The cells may be cylindrical, polyhedral, or they 
may present the characteristics of colloid cancer. Primary carcinomata 
of the gall bladder and larger ducts (Fig. 170) are not uncommon. Not 
infrequently the pancreatic and common ducts are both involved, and it 
is difficult to say whether the tumor is primary in the head of the pan- 
creas or in the gall duct. The bladder and ducts may also be secondarily 
involved in carcinomata of the stomach, liver, and duodenum. 
29 



THE SPLEEN. 



In studying the alterations produced in the spleen in disease, it is 
important to bear in mind the peculiar relations in which this organ 
stands to the blood-vessels and to the circulation. After passing through 
the various branches of the splenic artery and the limited systems of 
capillaries which are associated with it, the blood is not received at once 
into venous trunks, as in other parts of the body, but is poured directly 
into the pulp tissue. In this it circulates, under conditions which ren- 
der it liable to stagnation and undue accumulation, before it is taken 
again into well-defined vessels through the open walls of the cavernous 
veins. Moreover, these conditions, naturally unfavorable to undisturbed 
and vigorous circulation, are reinforced by the association of the splenic 
with the sluggish and often interrupted portal circulation. Bearing 
these considerations in mind, it will be in a measure plain why, as is in 
fact the case, the spleen should be more liable to alterations in size than 
any other organ in the body, and why, serving as it does as a sort of blood 
filter, it should be especially susceptible to the influence of deleterious 
materials of various kinds which in one way or another gain access to 
the blood. In this respect the relations of the spleen to the blood, and 
of the lymph nodes to the lymph, present suggestive analogies. 

WOUNDS, EUPTURE, AND H^EMOREHAGE. 

Wounds of the spleen are usually accompanied by extensive haemor- 
rhage, and are commonly fatal. Death usually occurs as the result of 
this haemorrhage, but it may be due to secondary inflammatory changes. 
Healing and recovery may, however, occur. 

Rupture of the spleen may be traumatic or spontaneous. In the for- 
mer case, it may be due to direct violence in the region of the organ or 
to injury to the thorax, falls, etc. In certain diseased conditions, the 
spleen is more liable to rupture than when it is normal. The rupture 
usually involves not only the capsule, but a more or less considerable 
portion of the parenchyma, and of course leads to haemorrhage. Spon- 
taneous rupture is rare, but may occur as the result of excessive enlarge- 



THE SPLEEN. 



379 



merit of the organ, as in typhoid fever, malaria, etc. — see below— or as 
the result of abscess. 

Haemorrhage.— Aside from the extensive haemorrhages from injury 
and rupture, the spleen may be the seat of small circumscribed haemor- 
rhages in various infectious diseases, although, owing to the peculiar dis- 
tribution of the blood, it is often very difficult to distinguish between a 
moderate interstitial haemorrhage and hyperaemia. 

DISTURBANCES OP THE CIRCULATION. 

Anamiia.— This may be associated with general anaemia, but it is not 
always present in this condition. When marked and unassociated with 
other lesions, the spleen is apt to be diminished in size, the capsule more 
or less wrinkled, the cut surface dry and lighter in color than normal, 
the trabecule unduly prominent. 




Fig. 171.— Congestion op the Spleen. 
6, dilated cavernous veins; c, trabecular of pulp tissue compressed between dilated cavernous 
veins; d, glomerulus. 

In this, as in other alterations simply of the blood-content of the 
spleen, neither the gross nor microscopical appearances are constant, 
because of the redistribution of blood which is apt to occur in the vis- 
cera after death. 

Hypermmia. — This may be passive, occurring when some obstruction 
to the portal circulation exists, most frequently in cirrhosis of the liver, 
but also with certain valvular lesions of the heart, emphysema, etc. 
The spleen is enlarged, but usually only to a moderate degree. The 
capsule is apt to be tense, and on section the pulp is dark red and may 
be soft or firm. The cavernous veins are dilated (see Fig. 171). Usually, 
when the lesion has existed for some time, there is a thickening of the 



380 THE SPLEEN. 

trabecule and reticular framework of the spleen, so that they are promi- 
nent on section. In other words, there is a chronic interstitial splenitis 
following the chronic congestion. 

Active Congestion of the spleen, which in most cases is scarcely to be 
differentiated from some forms of acute inflammation, and probably in 
many cases is associated with it, very frequently occurs in a great variety 
of acute and infectious diseases, such as typhoid fever, pneumonia, 
diphtheria, pyaemia, the exanthemata, etc; The spleen is enlarged, the 
capsule tense; on section, the pulp is soft, dark red in color, often swell- 
ing out from the cut surface and concealing the glomeruli and trabecu- 
le. Under these conditions, we may find the cavernous veins distended 
with blood, and the interstices of the pulp infiltrated with a variable, 
sometimes large quantity of red and white blood-cells. Or we may find, 
in addition to this, an increase in cells, which characterizes acute in- 
flammation or hyperplasia of the spleen (see below). 

Infarctions of the Spleen. — Embolic infarctions of the spleen are of 
frequent occurrence. They may be single or multiple, small or very 
large, sometimes occupying half of the organ. They are in general 
approximately wedge-shaped, corresponding to the area of tissue sup- 
plied by the occluded artery. They maybe hemorrhagic, i.e., red, or they 
may be white (see page 57). Infarctions, originally red, may become 
white after a time from changes in the blood-pigment. They may 
usually be seeu as dark-red, reddish-white, or white, hard, sometimes 
slightly projecting areas on the surface of the organ. Not infrequently 
the centre of the infarction is light in color, while the peripheral zone is 
dark red. A layer of fresh fibrin is sometimes seen over the surface of 
the infarction. The general as well as the microscopical appearances 
which they present depend largely upon the age of the infarction. In 
the earlier stages, the hemorrhagic infarctions present little more under 
the microscope than a compact mass of red blood-cells, among which 
may be seen the compressed necrotic parenchyma. The white infarction 
may show at first in a general way the usual splenic structure, but the 
entire tissue is in a condition of coagulation necrosis. The tissue may 
disintegrate and soften, and be more or less completely absorbed, with 
or without fatty degeneration. A zone of inflammatory tissue may 
appear around the infarction and upon the capsule, and this tissue, be- 
coming denser, assumes the characters of cicatricial tissue, and contracts 
around theunabsorbed remnant of the infarction, so that finally nothing 
may be left but a dense mass of fibrous tissue, which frequently draws in 
the surface, causing more or less distortion of the organ. This cicatrix 
may be pigmented or white. 

If the embolus be of an infectious, irritating nature, in addition to 
its mechanical effects there may be suppuration, gangrene, and the 



THE SPLEEN. 381 

formation of abscess. There may be perforation of the capsule and fatal 
peritonitis. 

INFLAMMATION". 

Acute Hyperplastic Splenitis (Acute Splenic Tumor). — The condi- 
tions under which acute inflammation of the spleen occurs have already 
been mentioned under active hyperemia, with which it is usually asso- 
ciated. It is a frequent though not a constant accompaniment of the 
acute infectious diseases, and seems in all cases to be a secondary lesion. 
The spleen is enlarged, sometimes to two or three times its normal size. 
On section, the pulp is soft, often almost diffluent, and projects upon the 
cut surface. The color is sometimes dark red, sometimes grayish red, 
or mottled red and gray. The trabecule and glomeruli are usually con- 
cealed by the swollen and softened pulp, but the glomeruli are some- 
times unusually prominent. 

Microscopical examination shows the marked increase in size to be 
due in part to the hyperemia; in part to a swelling and increase in the 
number of cells, sometimes of the pulp, sometimes of the glomeruli, or 
of both. We find large, multinucleated cells; cells resembling the ovoidal 
and polyhedral cells of the pulp, but larger and with evident division of 
the nuclei. Cells resembling leucocytes may be present in large num- 
bers, and larger and smaller cells in a condition of fatty degeneration, or 
containing pigment, are often seen. The elongated cells lining the cav- 
ernous veins may be swollen or increased in number. Kot infrequently 
larger and smaller cells are found which contain structures looking some- 
what like red blood-cells. In some cases, particularly in scarlatina, 
hyperplasia of the glomeruli is a prominent feature. In some cases, 
particularly in typhus and recurrent fevers, the cells of the glomeruli 
undergo marked degenerative changes, so that they may form small 
softened areas looking like little abscesses. Small necrotic areas, often 
associated with localized suppuration, are sometimes found in typhus 
and typhoid fever, scarlatina, etc., and may be due to infectious emboli. 
As the primary disease runs its course, the swelling of the spleen sub- 
sides, the capsule appears wrinkled, the color becomes lighter, and 
sometimes the organ remains for a long time, or permanently, small 
and soft. 

The cause of these marked changes in the spleen in infectious dis- 
eases is not understood. It seems probable that they are due to the 
lodgment in the organ of some deleterious materials which have found 
access to the blood. Whether these materials are bacteria, or products 
of the life processes of bacteria, or something entirely apart from these, 
we do not know. Bacteria have, indeed, in many cases been found in 
the organ under these conditions, but by no means with the frequency 
and abundance which the commonness and prominence of the lesion 
would lead us to expect if it were in all cases due to their presence. 



382 THE SPLEEN. 

Suppurative Splenitis (Splenic Abscess). — Small abscesses may be 
found in the spleen as the result of minute infectious emboli, and these 
may coalesce to form larger abscesses; but larger and smaller abscesses 
may form in the spleen without evidence of their embolic origin. 
Sometimes the entire parenchyma is converted into a soft, necrotic, puru- 
lent mass surrounded by the capsule. It is rare for simple infarctions 
to result in abscess, but it does occasionally occur. Abscess of the 
spleen may occur from the propagation of a suppurative inflammation 
to the organ from adjacent parts; from perinephritic abscesses, ulcer 
and carcinoma of the stomach, etc. Abscesses of the spleen may open 
into the peritoneal cavity, inducing fatal peritonitis, or, owing to an 
adhesive inflammation, the opening may occur into the post-peritoneal 
tissue, into the pleural cavity, lung, stomach, intestines, or it may open 
on the surface. On the other hand, the contents of the abscess may 
dry, shrink, and become incapsulated and calcified. Abscesses may 
occur in ulcerative endocarditis, pyaemia, typhoid fever, and more rarely 
in intermittent fever, and under a variety of other conditions whose 
nature is unknown to us. 

Chronic Indurative Splenitis (Chronic Splenic Tumor). — There 
may be, as we have already seen, a new formation of connective tissue in 
the spleen as a result of chronic congestion or infarctions, or about 
abscesses. But there is a more diffuse formation of connective tissue, 
usually in the nature of an hyperplasia, which occurs under a variety of 
conditions, and is now marked and extensive, and again comparatively 
ill-defined. It is always associated with more or less extensive changes 
in the parenchyma. In its most marked form it is found in chronic 
malarial poisoning, and under these conditions it may be found not only 
in persons who have suffered from repeated attacks of intermittent fever, 
but also in those who have not thus suffered but have resided in mala- 
rial regions. The enlarged spleen is often called " ague cake/' Simi- 
lar conditions, though usually less marked, may occur in congenital and 
acquired syphilis, from prolonged typhoid fever, and as a result of acute 
hyperplastic splenitis from various causes, and also in leukaemia and 
pseudo-leuksemia. 

The gross appearance of the spleen in chronic indurative splenitis 
varies greatly, both in the size of the organ and in the appearance of the 
section. The spleen may be enormously enlarged or it may be of about 
normal size. It is usually, however, enlarged. The capsule is usually 
more or less thickened, frequently unevenly so. The consistence is 
usually considerably increased, but this is not always the case. The 
color and appearance of the cut surface present much variation. It may 
be nearly normal or it may be grayish, or dark brown, or nearly black. 
The color may be uniform or the surface may be mottled. The glomeruli 
maybe scarcely visible or very prominent; the trabecule are in some 



THE SPLEEN. 383 

cases nearly concealed by the pulp; in others they are large, prominent, 
and abundant, so that the surface is crossed in all directions by an inter- 
lacing network of broader and narrower irregular bands, between which 
the red or brown or blackish pulp lies. 

Kot less varied are the microscopical appearances of the spleen under 
these conditions. In one class of cases, there is more or less uniform 
hyperplasia of both pulp and interstitial tissue. The parenchyma cells 
are increased in size and number; there may be swelling and prolifera- 
tion of the lining cells of the cavernous veins (see Fig. 172). The reti- 
culum of the pulp, as well as that of the glomeruli, and also the trabe- 
cular, are thickened. In another class of cases, the thickening of the 
reticular and trabecular tissue, either uniformly or in patches, is the 
prominent feature (Fig. 173), while the changes in the pulp are rather 
secondary and atrophic. In both forms, irregular pigmentation is fre- 




Fig. 172.— Chronic Indurative Splenitis. 
Showing swelling or proliferation of the lining cells of the cavernous veins. 



quent, the pigment particles being deposited either in the cells of the pulp 
or glomeruli, or in the new-formed interstitial tissue (Fig. 174). Finally, 
there are all intermediate forms of induration between those described, 
and the changes are by no means uniform in the same organ. When 
these spleens are large, they are liable to displacement. 

Syphilitic Splenitis. — This lesion may present itself as an indurative 
process due to the formation of new connective tissue, and present no 
distinct morphological characteristics. In rare cases, however, gummata 
may be present in connection with the new fibrous tissue; then the na- 
ture of the lesion becomes evident. 

Tubercular Splenitis. — This lesion is secondary, either to tubercular 
inflammation in some other part of the body, or is the result of the 
general infection in acute general miliary tuberculosis. The tubercles 
may be very numerous and still invisible to the naked eye, or they may 
be just visible, or as large as a pin's head or thereabouts, and very thickly 



384 



THE SPLEEN. 



strewn through the organ or sparsely scattered. In other cases, the 
tubercles are larger, sometimes as large as a pea, and they are then usually 
not very numerous. Microscopically they present the usual variety of 




Fig. 173.— Chronic Interstitial Splenitis. 
a, thickened capsule; b, thickened trabeculae ; c, dilated cavernous veins ; d, dense pulp tissue 
with obliterated cavernous veins. 

structure : sometimes as simple tubercle granula, sometimes as conglo- 
merate tubercles; they may consist simply of a collection of small sphe- 
roidal cells, or there may be larger polyhedral cells and giant cells, with 




Fig. 174.— Malarial Spleen. 
Showing thickening of the trabecular network of the pulp, with pigmentation of the pulp cells. 

a well-defined reticulum. Cheesy degeneration occurs under the usual 
conditions. Tubercle bacilli are usually present, particularly in the more 
acute forms, sometimes in small, sometimes in enormous numbers. 
They seem to be especially abundant in acute general miliary tuberculo- 
sis of children. These tubercles may be formed in the glomeruli, in the 
walls of the smaller arteries, in the pulp tissue, and in the trabecule and 



THE SPLEEN. 385 

capsule. Owing to the peculiar character of the spleen tissue, the earlier 
stages are not readily recognized, since simple collections of small sphe- 
roidal cells are not distinctly outlined against the normal tissue. There 
is frequently a moderate swelling of the spleen, owing to hyperemia 
and hyperplasia of the parenchyma. 

Perisplenitis. — Acute inflammation of the capsule of the spleen may 
occur as a part of a general or localized peritonitis, or as a result of 
lesions of the spleen itself, such as infarctions, abscesses, and acute hy- 
perplastic inflammation. Under these conditions, a fibrinous pellicle, 
with more or less pus, may be formed on the surface of the organ. 
Chronic perisplenitis, resulting in the production of new connective tis- 
sue, either in patches or as a more or less general thickening of the cap- 
sule, is of frequent occurrence. It may follow acute inflammation of 
the capsule, or be a part of general or localized chronic peritonitis. 
It is common in connection with chronic indurative splenitis, and it may 
occur from unknown causes. Sometimes the capsule is three or four 
mm. in thickness over a considerable area; sometimes very small nodular 
thickenings or papillary projections occur. As a result of this process, 
adhesions, sometimes very extensive, may form between the spleen and 
adjacent parts. The thickened capsule is sometimes more or less exten- 
sively calcified. 

Alterations of the Spleen in Leukmmia and Pseudo-Leukcemia. — The 
lesions of the spleen are essentially the same under both of these con- 
ditions. They consist, in general, of an hyperplasia, sometimes most 
marked in one, sometimes in another of the structural elements of the 
organ, but usually they all participate in the alterations. The changes 
which occur in the earlier stages are but little known . The gross ap- 
pearances of the spleen, as we find them in persons dying of either of the 
above diseases, present considerable variation. They are usually enlarged, 
and sometimes are ten or fifteen times the normal size. They are usually 
hard, but are sometimes of the ordinary consistence, or softer. The 
capsule is usually thickened and rough. The section of the spleen may 
be of a uniform dark-red color, but it is more frequently mottled red and 
gray. Sometimes the glomeruli are inconspicuous, but they are very 
often enlarged and prominent. They may be two to four mm. in dia- 
meter, and, owing to an infiltration of the arterial sheaths with lymph 
cells, may appear to the naked eye as grayish, round or elongated bodies, 
arranged along branching interrupted grayish streaks. The trabecula 
may be greatly thickened, as also the reticulum of the pulp, so as to be 
evident to the naked eye. Brown or black pigment may be collected 
around the glomeruli or in the pulp. Hemorrhagic infarctions or cir- 
cumscribed extravasations of blood may further complicate the picture. 

Microscopically the appearances are essentially the same as those 
above described in acute hyperplasia and in chronic interstitial splenitis, 



386 THE SPLEEN. 

depending upon the stage and variety of the disease. Owing to the great 
size which some of these spleens attain, they are liable to displacement, 
and they may interfere by pressure with the functions of neighboring 

organs. 

DEGENERATIVE CHANGES IN THE SPLEEN. 

Atrophy. — The spleen may become atrophied in old age; as a result 
of prolonged cachexia?, and in connection with profound and persistent 
anaemia; or, more rarely, from unknown causes. The capsule may be 
wrinkled and thickened, the color pale, the trabecula prominent, the 
consistency increased. The change is largely in the pulp, whose paren- 
chyma cells are decreased in number. 

Amyloid Degeneration. — This degeneration may affect the glomeruli 
or the pulp tissue, or both together. When confined to the glomeruli, 
the spleen may or may not be enlarged, and the cut surface is more or 
less abundantly sprinkled with round or elongated translucent bodies 
resembling considerably in general appearance the grains of boiled sago. 
These are the waxy glomeruli. Such spleens are often called "sago 
spleens." Microscopical examination shows that the degeneration is 
confined to the walls of the arteries, capillaries, and reticulum of the 
glomeruli, with atrophy and disappearance of the lymphoid cells. 

In other cases, either with or without involvement of the glomeruli, 
there is waxy degeneration of the blood-vessels and reticulum of the 
pulp, which may occur in patches or be general and more or less ex- 
cessive. If the alteration is general and considerable, the spleen is 
enlarged, its edges rounded, its consistence increased. On section, it 
appears translucent, and the distribution of the degenerated areas may be 
readily seen by holding a thin slice up to the light. The spleen may be 
alone affected, or there may be similar degenerations in other organs. 
The general conditions under which this lesion occurs, and the methods 
of staining and studying, are given on page 66. 

Pigmentation of the spleen may occur as the result of the decompo- 
sition of haemoglobin in the organ under a great variety of conditions: 
thus after haemorrhagic infarctions, small multiple haemorrhages, acute 
hyperplastic splenitis, etc. Or the pigment may be anthracotic and be 
brought to the organs from the lungs or bronchial glands (see page 61). 
Bile pigment may also be deposited in the spleen in jaundice. The pig- 
ment may lie in the walls of the smaller arteries, in the cells and reticu- 
lum of the pulp, or free in the latter tissue, or in the follicles. It is 
usually quite unevenly distributed. The pigment may be red, brown, 
or black. According to Weigert, anthracotic pigment maybe sometimes 
seen with the naked eye in the periphery of the glomeruli, as dark 
crescents. 



THE SPLEEN. 387 



TUMORS. 



Primary tumors of the spleen are rare. Small fibromata, sarcomata, 
and cavernous angiomata sometimes occur. Sarcomata and carcinomata 
may occur in the spleen secondarily either as metastatic tumors or by 
•extension from some adjacent part, as the stomach. Dermoid cysts are 
described, but are rare. Other larger and smaller cysts, whose mode of 
origin is in most cases obscure, not infrequently occur. 

PARASITES. 

Pentastomum denticulatum is not infrequently found in the spleen, 
usually incapsulated and calcified. Cysticercus is rare. EcJiinococcus 
is occasionally found, and, if the cysts are large or numerous, may cause 
more or less extensive atrophy of the organ. 

Various forms of bacteria have been found in the spleen. Micrococci 
have been found in pyaemia, small pox, ulcerative endocarditis, diphtheria, 
and under other conditions. The Bacillus anthracis occurs here in an- 
thrax; the B. tuberculosis in tubercular inflammation; and bacilli have 
been described in typhoid fever. SpirocUmte Obermeieri may be found in 
relapsing fever. 

MALFORMATIONS AND DISPLACEMENTS. 

. The spleen may be absent in acephalous monsters, and with defective 
develojmient of other abdominal viscera. Very rarely it is absent in 
persons who are otherwise perfectly developed. Small accessory spleens 
from the size of a hazelnut to that of a walnut are not infrequent. 
They usually lie close to the spleen, but may be considerably removed 
from it; thus they have been found imbedded in the head of the pan- 
creas. Two spleens of about equal size have been observed. The form 
of the spleen is subject to considerable variation. It may be made up 
of several distinct lobes. It may be displaced congenitally or as the re- 
sult of disease. It may be on the right side in transposition of the vis- 
cera. As the result of congenital defects in the diaphragm, the spleen 
may be found in the thorax; or in deficient closure of the abdominal 
wall it may, together with other abdominal viscera, be found outside of 
the body. 

The spleen may be pressed downward by any increase in the contents 
of the thorax. It may be fastened by adhesions to the concave surface 
of the diaphragm, so that its long axis is nearly horizontal instead of 
vertical. It may be displaced by changes in the contents of the abdomi- 
nal cavity. If the organ is increased in size, it frequently becomes 
tilted, so that its lower border reaches the right iliac region. If the 
ligaments are too long congenitally, or if they are lengthened by trac- 



38# THE SPLEEN. 

tion, and if the organ is at the same time increased in weight, it may 
become very movable. It may sink downward with its hilus turned 
upward; or it may be rotated on its axis, and, owing to torsion of the 
vessels thus produced, the organ may atrophy; or the pressure of the 
ligaments and vessels across the duodenum may cause occlusion of the 
gut. 



THE PA2TCEEAS. 



The diseases of the pancreas are, so far as we know, with a few ex- 
ceptions, of no great practical importance; that is, they do not often 
give rise to symptoms of disease or cause death, but the lesions are found 
in the bodies of persons dead from other diseases. It is probable, how- 
ever, that in many cases their apparent insignificance is due to our lack 
of knowledge of the interference with functiuns which lesions of the 
gland induce, and to the incomplete examination of the pancreas which 
is so common at autopsies. 

Haemorrhage into the substance of the pancreas may occur as the re- 
sult of injury; in the hemorrhagic diathesis; in connection with valvular 
diseases of the heart or interference with the portal circulation; or in 
connection with extensive fatty degeneration and fat necrosis of the 
organ. Such haemorrhages may be minute or extensive. Several cases 
of sudden death are recorded in which the only discoverable lesion was 
an extensive haemorrhage into the substance of the gland and the tissue 
about it. In these cases it has been assumed that death was caused by 
interference with the heart's action, through pressure on the solar plexus 
and semilunar ganglion, but it may be due to other causes (see below, Fat 
Necrosis). The haemorrhage may be moderate and limited to the pan- 
creas, or it may extend into the subperitoneal tissue for a considerable 
distance. 

Haemorrhage of the pancreas may be associated with acute inflamma- 
tory changes and with more or less extensive gangrene of the organ. 
The gangrenous pancreas may be more or less incapsulated; it may lie, 
bathed in pus, in the abdominal cavity; it may, by ulceration of the in- 
testinal wall, get into the gut and be discharged with other intestinal 
contents. 

INFLAMMATION. 

In some cases of typhoid fever, pyaemia, yellow fever, and other acute 
infectious diseases, the pancreas is red, swollen, and cedematous. Micro- 
scopically the most prominent lesion is a swelling and undue granula- 
tion of the glandular epithelium, and hyperaemia. This condition is 
known as Parenchymatous Pancreatitis. 



390 THE PANCREAS. 

Suppurative Pancreatitis is not very common, and may be primary 
or due to the extension of a suppurative inflammation from adjacent or 
distant parts of the body. There may be a diffuse infiltration of the 
organ, with pus cells or larger and smaller abscesses. The abscesses may 
open into the gastro-intestinal canal or into the peritoneal cavity. The 
causes of primary suppurative pancreatitis are often most obscure. It 
may be associated with fat necrosis and with haemorrhage and gangrene 
of the pancreas. 

Chronic Interstitial Pancreatitis (Cirrhosis of the Pancreas). — This, 
lesion consists in an increase of interstitial connective tissue, which may 
be general or confined to some particular portion of the gland. The 
organ is sometimes enlarged, sometimes smaller than normal. It is 
usually dense and hard; secondary atrophy of the parenchyma regularly 
occurs. It maybe due to chronic inflammatory processes in the vicinity 
of the organ. 

Syphilitic Inflammation. — Chronic interstitial pancreatitis is fre- 
quently found in congenital syphilis of the new-born, and the gross and 
microscopical lesions are similar to those above described. It is not defi- 
nitely established whether or not a similar lesion may be caused by 
acquired syphilis. Gummata are very rare in the pancreas, but have 
been described in congenital syphilis in very young children. 

Tubercular Inflammation. — Larger and smaller tubercles and tuber- 
cular, cheesy nodules are occasionally found in the pancreas in connection 
with acute general miliary tuberculosis or with tubercular inflammation 
in some other organ, particularly with that of adjacent lymph nodes, 
the lungs, and the intestine. 

DEGENERATIVE CHANGES IN THE PANCREAS. 

Atrophy of the pancreas may occur in old age, and as a result of 
pressure from tumors or other adjacent structures. Marked atrophy of 
the pancreas is found in a certain proportion of cases of diabetes mel- 
litus, but it is not constant. 

Fatty Degeneration of the parenchyma cells may occur, and in some 
cases is so extensive as to lead to nearly complete destruction of their 
protoplasm. 

Fatty Infiltration, which should be distinguished from fatty degene- 
ration, consists in the accumulation of fat in the interstitial tissue of the 
gland. This may be so excessive as to cause nearly entire destruction of 
the gland structures. Under these conditions, the outline of the organ 
may be preserved, the fat being inclosed by the capsule. 

Amyloid Degeneration. — This usually occurs in connection with 
similar degeneration in other organs, and is confined to the walls of the 
blood-vessels and the interstitial tissue. 

Fat Necrosis. — A very peculiar lesion of the fat tissue, most fre- 



THE PANCREAS. 



391 



quently seen in the fat tissue about the pancreas or between its lobules, 
but sometimes in fat tissue in other parts of the body, has been a few 
times described and called fat necrosis. White or yellowish nodules, 
varying from the size of a pin's head to that of a pea or larger, are seen 
imbedded in the fat, the central portion being often soft and grumous 
and readily squeezed out. They are sometimes calcified aud sometimes 
surrounded by a connective-tissue capsule. Microscopical examination 
shows degeneration and disintegration of the fat tissue (Fig. 175). They 
are most frequently found in marasmatic persons. When the lesion is 
extensive, according to Balser, it may cause death either directly or by 



mKwm^'M 









/fc''',-.:. : fc • '.JV.A 










0*W ,■■■-. 




^y^, 



Fig. 1?5.— Fat Necrosis in the Pancreas. 
Drawn from a specimen prepared by Or. Ira Van Gieson, and reported to the New York Patho- 
logical Society, 1888. 

inducing haemorrhage. Some of the extensive haemorrhages about the 
pancreas, above mentioned, may be caused in this way. 1 



TUMORS. 

Carcinomata are the most common and important of the tumors of 
the pancreas. They may be primary or secondary. Primary carcino- 
mata are most frequently found in the head of the organ, but may occur 

1 For a detailed consideration of acute iDflammation, haemorrhage, gangrene, and 
fat necrosis of the pancreas, with bibliography, consult Fits, Middleton Goldsmith 



Lecture for 1889 on 
Society, 1889. 



Acute Pancreatitis." Transactions New York Pathological 



392 THE PANCREAS. 

in other parts. The hard or scirrhous form is most common, but occa- 
sionally soft and succulent and colloid forms are found. They are 
liable to involve adjacent parts by continuous growth, and may form 
metastases in the liver, adjacent lymph nodes, etc. Secondary carcinoma 
in the pancreas may occur in carcinoma of the stomach, duodenum, and 
the gall ducts and gall bladder. As a result of carcinoma of the pancreas, 
aside from the extension of the growth, there may be pressure on the 
ductus choledochus, with jaundice; or on the pancreatic duct, with cystic 
dilatation; or pressure on the duodenum, with stenosis of the gut; or 
pressure on the vena cava, or portal vein, or superior mesenteric vein, 
etc.. with disturbances of the circulation. 

Concretions of carbonate and phosphate of lime are frequently found 
in the pancreatic ducts. They are usually multiple, small, whitish, 
smooth, or of rough and irregular shape. Sometimes, however, they 
reach a diameter of more than an inch. They consist chiefly of calcium 
phosphate and carbonate. Besides these free concretions, the walls of 
the ducts are sometimes incrnsted with salts of lime. Such concretions 
may produce dilatation of the pancreatic ducts and large cysts, or more 
rarely abscesses. 

Foreign Bodies. — Gall stones sometimes find their way into the pan- 
creatic duct. Ascarides have been found in the ducts in a considerable 
number of cases. 

Dilatation of the pancreatic ducts and the formation of cysts take 
place in several different ways. 

1. The entire duct may undergo a uniform cylindrical dilatation. 
With this cylindrical dilatation we sometimes find associated small sac- 
culi. 

2. There may be sacculated dilatations at some point in the ducts. 
These dilatations form cysts of large size, as large even as a child's head. 
Their walls frequently undergo degeneration and calcification. These 
cysts often become filled with blood, and may then be mistaken for an- 
eurisms. 

3. The small branches of the pancreatic duct may be dilated so as 
to form a number of small cysts. These cysts are filled with serum, 
mucus, pus, or a thick, cheesy material. 

MALFORMATIONS AND DISPLACEMENTS. 

The pancreas may be entirely absent in anencephalous and double 
monsters, and in congenital umbilical hernise. The pancreatic duct may 
be double; it may open into the duodenum at some distance from the 
biliary duct, or into the stomach. The head of the pancreas may be un- 
duly developed, and sometimes even completely separated from the rest 
of the organ, opening into the duodenum with a duct of its own. Occa- 



THE PANCREAS. 393 

sionally there is a small accessory pancreas situated beneath the serosa of 
the duodenum or stomach. 

The pancreas is so firmly bound down that its position is not often 
changed. Sometimes, however, it is found pressed downward by tight 
lacing, displaced by aneurisms, or contained in umbilical and diaphragm- 
atic hernias. 

30 



THE SALIVABY GLANDS. 



THE PAROTID, SUBMAXILLARY, AND SUBLINGUAL. 
INFLAMMATION. 

This condition is most frequent and important in the parotid. The 
epidemic disease known as mumps is most frequently confined to ♦ the 
parotid gland of one side, but the submaxillary and sublingual may be 
at the same time involved. The gland is swollen and there is often 
oedema of the mucous membrane of the mouth and pharynx. Very 
little is known of the actual minute changes which the gland undergoes 
in this disease. 

Acute parotiditis occasionally occurs as a secondary lesion in a variety 
of diseases, as in typhoid and scarlet fever, pyaemia, pneumonia, etc., 
and by propagation of inflammation from the mouth. Under these con- 
ditions the inflammation is usually suppurative, and frequently results 
in abscess or sloughing. The interstitial tissue of the gland is more or 
less densely infiltrated with pus cells, and the parenchyma cells may 
undergo fatty degeneration and disintegration. The inflammation may 
be confined to the gland or it may spread to adjacent parts, sometimes 
causing much destruction of tissue, and may give rise to inflammation 
of the brain or of the inner ear, or even to metastatic pyaemic abscesses 
in different parts of the body. Healing may occur, with the formation 
of salivary fistulae. 

The submaxillary gland may be involved with the parotid in the sup- 
purative inflammation. 

Acute suppurative inflammation of the connective tissue about the 
submaxillary gland is sometimes of serious import. Sloughing and gan- 
grene may occur, and are apt to spread to adjacent parts. Septicaemia, 
oedema of the glottis, or pneumonia may complicate the process and 
cause death. 

The sublingual gland is not often the seat of inflammation. 

Chronic inflammation, leading to the formation of dense interstitial 
tissue, sometimes occurs in the salivary glands. This may occur by it- 
self or follow an acute inflammation. 






THE SALIVARY GLANDS. 395 

The Excretory Ducts of the salivary glands may become inflamed from 
the presence of foreign bodies or of concretions formed in them. They 
may become occluded from the presence of calculi or as the result of 
inflammation, and may thus become widely dilated both in the main 
branches and in the finer ramifications. The dilatation of Wharton's 
duct to form larger and smaller cysts containing salivary fluid, some- 
times gives rise to very large and troublesome tumors which constitute 
one of the forms of ratiula. 

TUMORS. 

Fibromata are of occasional occurrence in the parotid. Chondromata, 
sarcomata and fibro-sarcomata, and myxomata, or more frequently mixed 
tumors formed of varied combinations of these, are of frequent occur- 
rence in the parotid, and of occasional occurrence in the submaxillary 
gland. These complex or mixed tumors are of more frequent occurrence 
in these glands than in any other part of the body, except possibly the 
ova*ry. They are sometimes rendered still more complicated in structure 
by a partially atypical glandular growth lending them an adenomatous 
character, and by the formation of cysts. Or they may present in parts 
a distinctly carcinomatous character. 

Fibrosarcoma and melano-sarcoma have been described. Primary 
carcinoma of these glands is very rare. 

One case of rhabdomyoma of the parotid gland, with evidences of aty- 
pical development of portions of the gland, has been described by one 
of us. 1 

PARASITES. 

Ecliinococcus has been observed in the parotid gland. 

1 Prudden, "Rhabdomyoma of the Parotid Gland." American Journal of the 
Medical Sciences, April, 1883. 



THE THTEOID GLAND. 



Hypermmia of the thyroid gland, often accompanied by considerable 
enlargement of the organ, may be the result of valvular disease of the 
heart; it occurs in Basedow's disease; it may be temporary or perma- 
nent, and in the latter case may give rise to the formation of new con- 
nective tissue. Haemorrhages may occur, causing pigmentation of the 
organ. 

Inflammation of the thyroid gland is not very common, and may 
occur from a variety of causes. It may result in the formation of larger 
and smaller abscesses, or in the production of new connective tissue. 
Tubercular inflammation, with the formation of miliary tubercles, is of 
infrequent occurrence. Syphilitic inflammation, with the formation of 
gummata, has been described, but is rare. 

Degeneration. — Colloid degeneration of the epithelial cells of the 
gland, and the filling of the alveoli with colloid material, is of common 
occurrence, and when occurring in moderate degree may be regarded as 
a normal event, since a certain amount of this change is found in many 
otherwise apparently normal glands. It may occur, however, to such an 
extent as to constitute a lesion (see below). 

Amyloid degeneration, particularly of the blood-vessels, is of infre- 
quent occurrence. 

TUMOKS. 

Among the most important of the lesions of the thyroid is the enlarge- 
ment of the organ commonly known as the goitre or struma. The 
enlargement of the gland may occur in several different ways, and in 
only a part of the cases is to be considered as a tumor. Thus, a simple 
hyperemia may, as above stated, cause considerable enlargement of the 
organ, and this is sometimes called Struma hypermmica. The true goitre, 
however, consists in the enlargement of the old and the formation of 
new gland alveoli, while with these changes there is very frequently asso- 
ciated a greater or less amount of colloid degeneration. When there is 
new formation of gland tissue, the growth has the character of an ade- 
noma. The hyperplasia may occur diffusely, so that the whole gland is 
more or less enlarged: or it may occur in the form of circumscribed 
nodules. When the colloid degeneration is prominent, so that the 



THE THYKOID GLAND. 397 

tumor lias a gelatinous look, it is called colloid struma. Accumulations 
of fluid, blood, colloid, etc., in the old or new-formed alveoli, may cause 
dilatation and atrophy of the walls of the alveoli, so that cysts, some- 
times of large size, are formed. Thus occurs the cystic struma. Again, 
the blood-vessels may undergo marked dilatation, so that we may have 
a telangiectatic struma ; or cavernous anyiomata may form within them. 
Very frequently all these varieties of lesions are present in the same goitre. 
The appearances may be rendered still more complex by the occurrence 
of haemorrhages and pigmentation, calcification, purulent or indurative 
inflammation, and by the not very infrequent association with carcinoma 
and sarcoma. The cause of goitre is not well understood. The growth 
is, as a rule, slow, but occasionally a very rapid enlargement occurs as 
the result of a sudden increase of the colloid degeneration. In many 
cases, even very large goitres give rise to but moderate inconvenience, 
but they may assume great significance by incroaching upon neighbor- 
ing parts. Thus death may be caused by pressure on the trachea, oeso- 
phagus, or on the large vessels. 

Sarcoma, either spheroidal or spindle-celled, may occur as primary 
tumors in the thyroid, either in otherwise normal glands or in connec- 
tion with struma. Melano-sarcoma has been observed. Secondary sar- 
comata are rare. 

Primary carcinoma, both glandular and scirrhous, occurs in the thy- 
roid, and, particularly in the softer forms, may spread to adjacent parts, 
and occasionally form distant metastases. 

PARASITES. 

Echinococcus cysts have been found in the thyroid. 

The thyroid gland is sometimes very small, either as the result of 
atrophy or as a congenital deficiency. This is most marked in the con- 
dition called myxcedema (see below). 

MYXEDEMA. 

This disease occurs most frequently in middle-aged women, and its 
cause is unknown. The skin of the face is apt to be swollen and waxy, 
causing a peculiar and rather characteristic appearance of the features. 
The skin of the body is apt to be dry and rough, and the hair may fall 
out. Perspiration is, as a rule, diminished. The mental condition is 
dull, and loss of memory and insanity may occur. Bodily movement and 
speech are apt to be impaired. 

The fat tissues may be atrophic, and the subcutaneous tissue has been 
shown in some, though not all, of the cases to contain an unusual amount 
of mucin. In some cases, the fibres of the upper layers of the corium are 
crowded apart by fluid. 



398 THE THYROID GLAND. 

The most marked and constant lesion in this disease is an atrophic 
condition of the thyroid gland. The parenchyma of the gland is more 
or less completely replaced by fibrillar connective tissue and by new- 
formed reticular tissue resembling the lymphatic tissue of the lymph 
nodes. 

The general appearance of the atrophied thyroid gland is shown in 
Fig. 176. 

In a case reported by Hun, which one of ns has examined, the lobes 
of the thyroid measured less than one-half of an inch in diameter, and 
the entire gland weighed only about 7.2 gm. (112 grains). 

In addition to the lesion of the thyroid, there are apt to be chronic 
endarteritis and chronic diffuse nephritis. In some cases there is an 
accumulation of small spheroidal cells about the smaller blood-vessels in 
various parts of the body, and also petechial haemorrhages. 

fill WMi 

§ !#•) mm 

■;- . :■■■■■■■■■■: -■ 

% "Mm'- p'ji 

Fig. 176.— Section of the Atrophied Thyroid Gland in Myxcedema. 
a, interstitial tissue; &, atrophied lobules with small spheroidal-celled or lymph tissue in their 
peripheries. 

While the atrophy of the thyroid is the most marked and frequent 
lesion in this disease, our lack of knowledge about the function of this 
gland prevents a definite conception as to the relationship of this change 
to the symptoms. 

By the destruction of the thyroid from disease, or as the result of 
its removal in men and animals, a condition considerably resembling 
myxoedema is apt to be induced. 

Myxoedema appears to be identical with that condition which has 
been described as cachexia sfrumipriva. 1 

1 For detailed descriptions of myxoedema, and the literature, see Hun and Prudden, 
" Myxoedema," Am. Jour. Med. Sciences, July and August, 1888, and "Report on 
Myxoedema" in Supplement to vol. xxi. Clinical Society Transactions, London, 1888. 




THE THYROID GLAND. 399 

THYMUS GLAND. 

The thymus occasionally but not usually persists until youth or mid- 
dle age instead of undergoing the usual developmental atrophy. 

Small hcemorrhages are described in the thymus of young children as 
the result of venous congestion in asphyxia, etc. They may also occur 
in the hasmorrhagic diathesis. 

Suppurative Inflammation of the thymus is of occasional occurrence, 
and is usually secondary to a similar inflammatory process in some other 
part of the body. 

Tubercular and syphilitic inflammation of the thymus are described. 
The sarcomata are the most common tumors of the thymus. 



THE SUPKAKEJ^AL CAPSULES. 



MALFORMATIONS. 



In acephalic and other monsters, the suprarenal capsules may be 
atrophied or entirely absent. Sometimes in well-formed adults these 
organs cannot be discovered. 

There may be little rounded nodules loosely attached to the surface 
of the capsules and having the same structure. 

If one of the kidneys is absent or in an abnormal position, its supra- 
renal capsule usually retains its proper position. 

HAEMORRHAGE. 

In children, soon after birth, it is not very infrequent to find large 
haemorrhages in one of the capsules, converting it into a cyst filled with 
blood. The same lesion has been observed in a few cases in adults. 

THROMBOSIS. 

Klebs describes a case of capillary thrombosis of the cortex in both 
capsules in a woman after excision of the knee joint. 

INFLAMMATION. 

The most frequent lesion of the suprarenal capsules is tubercular in- 
flammation. They are usually increased in size, their surfaces are smooth 
or nodular. The normal structure of the gland is lost, and is replaced 
by tubercle tissue, connective tissue, and cheesy matter (see Addison's 
Disease). 

Suppurative Inflammation, with the formation of abscesses, has been 
seen in a few cases. 

DEGENERATION. 

Fatty Degeneration of the cortical portion of the capsules is the rule 
in the adult. It sometimes occurs in nodular areas. In children under 
five years of age, it is a pathological condition. 

Amyloid Degeneration may involve both the cortical and medullary 
portions. In the cortex, it usually involves only the walls of the blood- 



THE SUPRARENAL CAPSULES. 401 

vessels; in the medulla, both the blood-vessels and the cells of the paren- 
chyma may undergo this degeneration. The capsules are usually firm 
and of a grayish, semi-translucent color. 

TUMORS. 

Carcinoma of the suprarenal capsules is not common. It may be 
primary, but is much more frequently secondary. Either one or both of 
the capsules may be the seat of the new growth. 

Sarcoma occurs as a primary and secondary growth. Probably many 
of the older cases described as cancers were really sarcomata. 

Cylindroma. — Klebs describes a growth of this character in one of 
the capsules, secondary to a tumor of the same kind in the supra-orbital 
region. He gives to such tumors the name of lymphangioma caver- 
nosum. The exact character of these growths is still obscure. They 
consist of irregular follicles and cavities, lined with epithelium, and con- 
taining peculiar hyaline, structureless bodies. 

Cysts are found both single and multiple. They are usually situated 
in the cortex. 

Neuroma. — A ganglionic neuroma has been described by Weichsel- 
baum. 1 

Glioma has been described as occurring in the medullary region. 

An hyperplasia of the gland tissue, with fatty degeneration in the 
form of circumscribed nodules, is described by Virchow. 

1 Virch. Archiv, Bd. 85, p. 554 
31 



THE URINARY APPARATUS. 



THE KIDINTEYS. 



MALFORMATIONS. 



Entire absence of both kidneys is sometimes associated with great 
malformation of the entire body. Snch foetuses are not viable. 

Absence of one kidney is not uncommon, the left kidney being more 
frequently absent than the right. The absence of the kidney may be 
complete, the ureter being also absent; or there may be a little mass of 
connective tissue and fat to represent the kidney, and a ureter running- 
down to the bladder. The single kidney which is present is usually 
much enlarged. It may be in its natural position or displaced down- 
ward. 

Since the extirpation of the kidney has been practised by surgeons, it 
has been found that absence of one kidney is more common than was 
formerly believed. 

When both kidneys are present, one of them may be much larger than 
the other. 

Sometimes one kidney will have two pelves or two ureters. 

A rather frequent malformation is the so-called horseshoe kidney. 
The lower ends of the kidneys are joined together by a commissure. 
The commissure is usually composed of kidney tissue, but sometimes of 
connective tissue. The two kidneys may be normal, except for the com- 
missure; or their shape, the arrangement of the vessels and ureters, and 
the position, may be unnatural. 

The two kidneys may be united throughout so as to look like a single 
misshapen kidney with two or more pelves and irregular blood-vessels. 
The united kidneys may be both situated on one side of the vertebral 
column or in the pelvis. 

CHANGES IN POSITION. 

The kidneys may be placed in an abnormal situation, in which they 
are either fixed or movable. 

The change in position is either lateral or downward. When dis- 



THE URINARY APPARATUS. 403 

placed downward, the kidney may be over the sacrum or below this in 
the cavity of the pelvis. The vessels also have an irregular origin and 
distribution. The kidney is firmly attached in its abnormal position. 

Movable or wandering kidneys are found in adult life as a result of 
tight lacing, of pregnancy, of over-exertion, and of unknown causes. 
They are more frequent in females than in males. The right kidney is 
the one more frequently affected. The blood-vessels become lengthened 
and the attachments of the kidney longer and looser. 

bright's disease. 

This name is used as a convenient term to group together a certain 
number of diseases of the kidney. This group may be subdivided as 
follows : ■ 

I. Acute Bright's Disease. 

1. Acute Congestion of the Kidney. 

2. Acute Degeneration of the Kidney. 

3. Acute Exudative Nephritis. 

4. Acute Diffuse Nephritis. 

II. Chronic Bright's Disease. 

1. Chronic Congestion of the Kidney. 

2. Chronic Degeneration of the Kidney. 

3. Chronic Diffuse Nephritis with Exudation. 

4. Chronic Diffuse Nephritis without Exudation. 

1. Acute Bright's Disease. 

1. Acute Congestion of the Kidney. — This change in the kidneys we 
know rather from clinical than from anatomical experience. 

It is caused by the ingestion of some poisons, especially cantharides, 
by severe injuries, and by surgical operations. It also occurs as a tem- 
porary condition in the course of chronic Bright's disease. 

The characteristic symptom is diminution in the quantity, or sup- 
pression, of urine. 

2. Acute Degeneration of the Kidney. — This is an acute change in 
the kidneys, characterized by degeneration or death of the epithelium of 
the tubes and of the capsule cells of the glomeruli. It is also called 
" parenchymatous inflammation.'" 

It is caused by severe inflammations of other parts of the body; by 
the presence in the body of the poisons of the infectious diseases; and 
by the ingestion of poisons, especially of arsenic, mercury, and phos- 
phorus. 

After death the gross appearance of the kidneys varies with the in- 
tensity of the morbid process and with the presence or absence of secon- 
dary changes on the part of the blood-vessels. In the milder cases the 



404 



THE URINARY APPARATUS. 



kidney is a little swollen and the cortex is pale; in the severe cases the 
kidney is much enlarged and the cortex is either white or congested. 

The changes in the renal epithelial cells are: a simple swelling of the 
cell body, especially of its network, causing it to look larger and more 
opaque and to take on irregular shapes; an infiltration of the cell bodies 
with granules of albuminoid matter and fat; a death of the cells, which 
may take the form of coagulation necrosis or of a disintegration and 
crumbling of the cell bodies; a desquamation of the dead cells; a forma- 
tion of hyaline masses in the cells; a growth of new cells to take the place 
of the dead epithelium. All these changes are most marked in the con- 
voluted tubes (Fig. 177). 







* , * *-^h?A ^~< -est 



Fig. 177. — Acute Degeneration of the Kidney (Acute Parenchymatous Nephritis). 
From a case of yellow fever, a, the swollen and granular epithelium peeling off and disinte- 
grating; 6, hyaline material in the lumen of the tubule. 



If the degeneration or death of the renal epithelium is extensive and 
produced quickly, it is often accompanied by congestion of the blood- 
vessels and exudation of serum. The congestion will be found after 
death, and also casts in the straight tubules. 

3. Acute Exudative Nephritis. — This is frequently a primary ne- 
phritis, either occurring after exposure to cold or without discoverable 
cause. It complicates scarlatina, measles, diphtheria, typhoid fever, 
acute general tuberculosis, pneumonia, acute endocarditis, acute peri- 



THE URINARY APPARATUS. 



405 



tonitis, dysentery, erysipelas, diabetes, and many other of the infec- 
tious diseases and severe inflammations. It is one of the forms of 
nephritis which complicate the puerperal condition. It has been ob- 
served in local epidemics, apparently due to the presence of pathogenic 
bacteria in the kidney. 

The nephritis has the ordinary characters of an exudative inflamma- 
tion: congestion, an exudation of blood plasma, an emigration of white 
blood-cells, and a diapedesis of red blood cells; to which may be added 
swelling or necrosis of the renal epithelium and changes in the glome- 
ruli. 




Fig. 178.— Acute Nephritis, x 850 and reduced. 
Paris green 20 hours before death. 

In the milder cases we find the inflammatory products — serum, casts, 
white and red blood-cells — in the urine. But in the kidneys after death 
we find no lesions, unless it may be a few casts in the straight tubes. 
The morbid process is confined to the blood-vessels of the kidney, and 
its only result is the exudation into the renal tubules. 

In the more severe cases, we find the kidneys large and smooth, the 
cortex thick and white, or white mottled with red, or the entire kidney 
intensely congested. If the stroma is infiltrated with serum, the kidney 
is succulent and wet; if the number of pus cells is very great, there will 
be little, whitish foci in the cortex. 



406 



THE URINARY APPARATUS. 



There are, besides the exudation, changes in the tubes, the stroma, 
and the glomeruli. All the changes are most marked in the cortical 
portion of the kidney. 

In the tubes, the epithelium may be flattened, or swollen, opaque, 
and detached from the walls of the tubes. There may be a uniform, 
symmetrical dilatation of all the cortex tubes. The tubes may be empty 
or they may contain coagulated matters in the form of irregular masses 
and of hyaline cylinders. The irregular masses are found principally in 
the convoluted tubes; they seem to be formed by a coagulation of sub- 




Fig. 179.— Acute Nephritis occurring with Acute General Tuberculosis, X 850 and reduced. 

stances contained in the exuded blood-plasma, and are not to be con- 
founded with the hyaline globules so often found in normal convoluted 
tubes. 

The hyaline cylinders are more numerous in the straight tubes, but 
are also found in the convoluted tubes. They are also formed of 
matter coagulated from the blood-plasma, and are identical with the casts 
found in the urine. The tubes may also contain red and white blood- 
cells. 

In some cases there is an excessive emigration of white blood-cells. 
This excessive emigration is not necessarily attended with exudation 



THE URINARY APPARATUS. 



407 



of the blood-serum, and so the urine of these patients may contain no 
albumin. 

The white blood-cells are not found equally diffused throughout the 
kidney, but are collected in foci in the cortex. These foci may be very 
minute or attain a considerable size. They do not resemble the sup- 
purating foci seen with embolism or with pyelo-nephritis. 

In the glomeruli we find considerable changes. The cavities of the 
capsules may contain coagulated matter and white and red blood-cells, 
just as do the tubes. The capsular epithelium may be swollen, some- 
times so much so as to resemble the tubular epithelium, and this change 




Fig. 180.— Acute Nephritis. 
Showing the swelling and growth of cells in and on the capillaries of a glomerulus in a case 
of scarlatina. 

is most marked in the capsular epithelium near the entrance of the 
tubes. 

The most noticeable change, however, is in the capillary tufts of the 
glomeruli. These capillaries are normally covered on their outer sur- 
faces by flat, nucleated cells, so that the tuft is not made up of naked 
capillaries, but each separate capillary throughout its entire length is 
covered over with these cells. There are also flat cells which line the 
inner surfaces of the capillaries, but not continuously, as is the case with 
capillaries in other parts of the body. 



408 



THE URINARY APPARATUS. 



In exudative nephritis, the swelling and growth of cells on and in the 
capillaries change the appearance of the glomeruli. They are larger, 
more opaque; the outlines of the main divisions of the tufts are visible, 
but those of the individual capillaries are lost. This change in the 
appearance of the glomeruli is due to the swelling and growth of the 
cells on and in the capillaries (Fig. 180). 

In very severe cases, the growth of the cells on the tufts is so con- 
siderable that they form large masses of cells between the glomerulus 
and its capsule. 

The walls of the arteries in the kidneys may be thickened by a 
swelling of their muscular coats. 

Acute exudative nephritis is regularly a transitory lesion. It may, 




Fig. 181.— Acute Diffuse Nephritis. 
From a case of scarlatina, a. swollen capsular epithelium; b, proliferation of tuft cells; c, 
compressed tuft; d, swollen stroma infiltrated with cells; e, dilated convoluted tubules; g, swollen 
epithelium peeling off; h, hyaline casts. 



indeed, be so severe as to destroy life in a short time. But, as a rule, if 
the patients do recover from it, they recover completely, and the kidneys 
return to their natural condition. 

4. Acute Diffuse Nephritis. — This is the most serious and important 
of all the forms of acute nephritis, not only for the reason that it in- 
volves so much of the structure of the kidney, but because its lesions 
are from the first of a permanent character, and because disturbances of 
the general circulation are so frequently associated with it. 

It is one of the forms of scarlatinal nephritis; it occurs early and late 
in the course of diphtheria; it is the most important variety of the 



THE UEINARY APPARATUS. 409 

nephritis of pregnancy, and it is especially frequent as a primary nephri- 
tis, with or without a history of exposure to cold. The course of the 
inflammation is acute or subacute. If it does not prove fatal as an acute 
inflammation, it regularly continues as a chronic nephritis. 

The changes in the kidneys are extensive and well marked. 

The kidneys are large, at first smooth, later sometimes a little rough- 
ened; the cortical portion is thick, white, or mottled with yellow or red, 
or congested; the pyramids are red. 

In these kidneys we find the same lesions as have been described as 
belonging to exudative nephritis, but with two additional changes — 
changes which are found in the earliest stages of the inflammation, and 
which give the characteristic stamp to the lesion: first, a growth of con- 
nective tissue in the stroma; second, a growth of the capsule cells of the 
glomeruli. 

These changes do not involve the whole of the kidney, but symmet- 
rical strips or wedges in the cortex which follow the line of the arteries. 
These wedges are small or large, few or numerous, regular or irregular, 
in the different kidneys. But in every wedge we find the same general 
characters: one or more arteries, of which the walls are thickened; glo- 
meruli belonging to these arteries, with a large growth of. capsule cells 
compressing the tufts; a growth of new connective tissue in the stroma 
around and parallel to the arteries. Between the wedges we find at first 
only the changes of exudative nephritis; later, a diffuse growth of con- 
nective tissue (Fig. 181). 

If the nephritis is of acute type and recent, the new tissue between 
the tubes consists largely of cells; if the nephritis is of subacute type 
and longer duration, the tissue is denser and has more basement sub- 
stance. Where the growth of new tissue is abundant, the tubes become 
small and atrophied. 

The exudation from the blood-vessels is very considerable, so that the 
urine contains large quantities of albumin, many casts, and red and 
white blood-cells. 

II. Chronic Bright'' 's Disease. 

1. Chronic Congestion of the Kidney. — This change in the kidney 
may be produced by any causes which interfere with the circulation of 
the blood and produce venous congestion. The most common cause is 
valvular disease of the heart. 

The kidneys are of medium size or large. Their weight is increased; 
they are hard and uniformly congested; their surfaces are smooth. The 
epithelium of the cortex tubes is opaque, flattened, or swollen. The 
glomeruli show a dilatation of the capillaries, with more or less thicken- 
ing of their walls, and swelling of the cells which cover their walls. In 
the stroma there is nothing but some exaggeration of the subcapsular 
32 



41 THE URINARY APPARATUS. 

areas of connective tissue which are found in normal kidneys. The 
arteries are normal, the pyramid veins are congested and sometimes 
dilated. 

The effect of this lesion of tl e kidney is simply to diminish the quan- 
tity of the urine, its quality remaining good. 

2. Chronic Degeneration of the Kidney. — This condition is produced 
by long-continued disturbances of the circulation due to heart disease, 
empyema, and similar conditions, and to causes which impair the gen- 
eral health, such as alcoholism. 

The kidneys are, as a rule, considerably increased in size, weighing 
together from sixteen to twenty ounces; but occasionally their size is 
much diminished. Their surfaces are smooth; the cortical portion is 
thickened, of pink or white color; the pyramids are red. 

The epithelium of the cortex tubes is swollen, coarsely granular, or 
infiltrated with fat. If the kidney lesion is due to disturbances of the 
circulation, the capillaries of the glomeruli are dilated. There are no 
changes in the stroma or arteries. At times there is a small exudation 
from the blood-vessels, and casts and albumin appear in the urine. 

These changes in the kidney do not, as we might expect, change 
materially the composition of the urine. This continues to contain its 
full relative quantity of solid matter. 

It is very difficult to find a satisfactory plan of classifying the remain- 
ing forms of chronic Bright's disease. The changes found in all the 
kidneys are of much the same kind, although differing in degree. The 
clinical symptoms also are of much the same character in all the patients. 
And yet it has always been felt by clinical observers that there are three 
main forms of chronic B right's disease, and that there must be anato- 
mical differences to correspond to these forms. 

It has seemed to me that the simplest form of classifying these kid- 
neys is according to the presence or absence of exudation from the blood- 
vessels, and that, of the non-exudative cases, we may distinguish the 
more active and the very slow cases. In this way, we may speak of 
chronic diffuse nephritis with exudation; chronic diffuse nephritis 
without exudation; and chronic diffuse nephritis of very slow develop- 
ment. 

3. Chronic Diffuse Nephritis with Exudation. — This follows acute 
and subacute diffuse nephritis and chronic degeneration of the kidney, 
or it is from the first a chronic lesion. 

There is a certain activity about the morbid process, although the 
patients may not die until after a number of years. The disposition to 
dropsy, to anaemia, to loss of flesh and strength, is very marked. 

The specific gravity of the urine is low, but yet often not below 1020. 
The excretion of urea is diminished. The quantity of urine is increased, 
except at the times when the kidney is congested. Albumin in large 



THE URINARY APPARATUS. 411 

quantities is present, except at the times when the inflammation seems 
nearly to have subsided. White and red blood-cells are present from 
time to time when the nephritis becomes more intense. 

Most of the kidneys are increased in size. The surface is smooth or 
roughened, or nodular. The cortex is thick and white, or gray, or 
mottled with various combinations of white, yellow, gray, and red. Less 
frequently the kidneys are small, the cortex is thick, white or gray. 
Occasionally the size and gross appearance are hardly to be distinguished 
from those of a normal kidney. 

The changes in the kidney are : a large exudation from the blood- 
vessels, most of which is mixed with the urine, while a part is found in 
the kidney tubules in the form of coagulated matter and casts; degene- 
ration of the renal epithelium; a growth of new connective tissue in 
the stroma between the tubes; swelling and multiplication of the tuft 
cells of the glomeruli; obliteration of the capillaries of the glomeruli, 
sometimes waxy degeneration of these capillaries. In a considerable 
number of these kidneys, the walls of the arteries are thickened or the 
seat of waxy degeneration. 

As regards the exact detail of the development of these changes, the 
variety is almost without limit. The more ordinary types of the lesion 
are as follows : 

(a) The kidneys are changed as they are in acute diffuse nephritis. 
There are the same cortical wedges containing new connective tissue, 
atrophied tubes and glomeruli, arteries with thickened walls, and glo- 
meruli with a new growth of capsule cells. Between the wedges the 
tubes are more or less dilated; their epithelium is flattened; there is a 
diffuse growth of connective tissue in the stroma; the tuft cells of the 
glomeruli are increased in size and number. 

(b) There is a diffuse growth of connective tissue in the stroma of the 
cortex. The tubes are more or less dilated, their epithelium is flattened. 
The tuft cells of the glomeruli are increased in size and number. 

(c) There are irregular areas, just beneath the capsule, composed of 
connective tissue, atrophied tubes, and atrophied glomeruli. In the cor- 
tex between these areas there are more or less degeneration of the epi- 
thelium, irregular thickening of the stroma, deformities of the tubes, 
growth of tuft cells, and atrophy of the glomeruli. 

(d) There is waxy degeneration of the glomerular capillaries and ar- 
teries added to the other lesions. 

(e) In addition to the other lesions there is extravasated blood in the 
tubes. 

4. Chronic Diffuse Nephritis without Exudation. — The difference be- 
tween the more rapid and the very slow forms of chronic nephritis with- 
out exudation is a clinical one. The lesions are the same in both sets 
of cases. 



412 



THE URINARY APPARATUS. 



In the more rapid cases, the ordinary symptoms are loss of flesh and 
strength, dyspnoea, contraction of the arteries, headache, sleeplessness, 
convulsions, and coma. The clinical history extends over a few months 
or over many years. The urine is generally abundant and of low speci- 
fic gravity and without albumin. At the times when the patient is 
worse, the urine is apt to be diminished and to contain a little albumin. 

In the slow cases, there may be no symptoms, except a gradual fall in 
the specific gravity of the urine, up to the time of the patient's death; or 
from time to time some of the symptoms just mentioned are developed. 

After death many of these kidneys do not differ in their gross ap- 
pearance from normal kidneys. If the disease is far advanced, however, 




Fig. 182.— Chronic Diffuse Nephritis. 
Atrophied kidney, showing small patch of new connective tissue with atrophy of inclosed tubules. 
a, new connective tissue ; b, atrophied tubule containing hyaline cast; c, tubule with epithelium 
peeling off; d, thickened capsule of glomerulus. 

most of them are atrophied, with adherent capsules and nodular surfaces. 
Less frequently these kidneys are very large. 

The most prominent feature of the lesion is the growth of new con- 
nective tissue in the stroma (Fig. 182). This is confined to areas of 
irregular shape in the cortex, or there is also a diffuse growth of con- 
nective tissue in the cortex and in the pyramids. 

The epithelium of the tubes is degenerated. Where there is much 
new connective tissue the tubes are atrophied and compressed. In other 
places the tubes are irregularly dilated, sometimes so much so as to 
form cysts. 



THE URINARY APPARATUS. 



413 



Of the glomeruli, some have their capsules thickened, some show a 
swelling and growth of the tuft cells, some are completely atrophied; in 
some the capillaries undergo waxy degeneration (Fig. 183). 

There are very often changes in the arteries. There may be only 
thickening of the muscular coat, with no change in the size of the 
lumen of the artery. There may be a diffuse connective-tissue thicken- 
ing of the entire wall of the artery, with moderate diminution of its 
lumen. There may be thickening of the inner coat so great as partly 
or completely to close the artery. 




Fig. 183.— Waxy Degeneration op Tuft Capillaries. 

a, the tuft is completely transformed into a waxy mass; b, portions of tuft waxy; c, tuft capil- 
laries normal ; d, convoluted tubule with disintegrating epithelium . 



SUPPURATIVE NEPHRITIS AND PYELO-NEPHRITIS. 

Suppurative inflammation of the kidney may be produced by injuries,, 
by emboli, by cystitis, and may occur without discoverable cause. 

1. Suppurative Nephritis from Injury. — G-unshot wounds, incised 
or punctured wounds, falls, blows, and kicks are the ordinary traumatic 
causes. If the injury is a very severe one, it usually causes the death of 
the patient in a short time; if it is less severe, suppurative inflammation 
is developed. The inflammatory process may be diffuse, so that nearly 
the whole of one or of both kidneys is converted into a soft mass com- 
posed of pus, blood, and broken-down tissue; or it is circumscribed and 
one or more abscesses are formed in the kidney. 



414 THE URINARY APPARATUS. 

2. Embolic Abscesses. — In pyaemia and in malignant endocarditis, 
small infectious emboli find their way into the arteries of the kidneys 
and produce necrosis of small areas of tissue, with surrounding zones of 
suppurative inflammation, The entire kidney is enlarged and congested, 
and is dotted with little white foci surrounded by red zones. The foci 
are formed by an infiltration of pus cells between the tubes, with more 
or less degeneration of kidney tissue. Colonies of micrococci are some- 
times, but not always, found in the Malpighian tufts and in the abscesses 
(see Fig. 31, page 93). 

3. Idiopathic Abscesses. — Sometimes abscesses of one or both kidneys 
are met with which have existed for a long time and for which no 
cause can be discovered. After death the kidney is found changed into 
a sac full of pus and surrounded by fibrous tissue. The pelvis and 
calyces are dilated, and their walls are thickened. The connective tis- 
sue around the kidney, and its capsule, are also thickened. Suppurat- 
ing sinuses may extend from the kidney into the surrounding soft parts. 

4. Suppurative Pyelo- Nephritis with Cyditis. — Both kidneys are 
usually affected. The mucous membrane of the pelvis is congested, 
thickened, and coated with pus or with patches of fibrin. Scattered 
through the kidneys are abscesses and foci of pus of different sizes. The 
smallest are hardly visible to the naked eye, but with the microscope we 
find small collections of pus cells between the tubes, with swelling and 
degeneration of the renal epithelium. The larger purulent foci look 
like white streaks or wedges parallel to the tubes and surrounded by 
zones of congestion. The larger abscesses replace considerable portions 
of the kidney tissue. 

The ureters are sometimes inflamed, their walls are thickened, their 
inner surfaces are coated with pus or fibrin. 

The bladder is always inflamed, and this is the primary lesion, to 
which the kidney lesion is secondary. It may present any of the lesions 
of acute or chronic cystitis. 

CHRONIC PYELONEPHRITIS. 

Chronic cystitis or calculi in -the pelvis of the kidney may set up a 
chronic inflammation which involves both the pelvis and calyces and 
the kidney tissue. The mucous membrane of the pelvis and calyces is 
thickened, the epithelial layer is changed, there is a growth of granula- 
tion tissue beneath the epithelium, and there may be little polypoid out- 
growths. The surface of the mucous membrane is coated with pus or 
fibrin, or the cavity of the pelvis is dilated and distended with purulent 
serum. 

The kidney itself is the seat of a chronic interstitial inflammation 
with the production of new connective tissue, and sometimes of pus with 
obliteration of the renal tubules. 






THE URINARY APPARATUS. 415 



TUBERCULAR NEPHRITIS. 



This lesion is usually, though not always, associated with tubercular 
inflammation in other parts of the genito-urinary tract. 

It is usually unilateral, occurring most frequently on the left side. 
The process may commence in the kidney or in some other part of the 
genito-urinary tract. If only one kidney is involved, the other is apt to 
become the seat of chronic diffuse nephritis, with waxy degeneration of 
the walls of the arteries. The tubercular inflammation may occur in a 
kidney already the seat of chronic inflammatory changes. 

The lesion seems to begin in the mucous membrane of the pelvis and 
calyces, and extend from thence first to the pyramidal and afterward to 
the cortical portion of the kidneys. In the mucous membrane of the 
pelvis and calyces, there is a growth of granulation tissue studded with 
tubercle granula in the stroma, while the epithelial cells proliferate, be- 
come deformed, and desquamate. This process is often rapidly succeeded 
by cheesy degeneration of all the inflammatory products. 

In the kidney, there is the same production of granulation tissue and 
tubercle granula, which soon undergo cheesy degeneration, the degene- 
ration involving the adjacent kidney tissue. In addition to this, there 
is in the rest of the kidney chronic interstitial or suppurative inflamma- 
tion. So the entire kidney is enlarged, portions are in the condition of 
cheesy degeneration or have sloughed away, while the rest of the kidney 
is dense and hard. Or, if suppuration takes place, the kidney is hollowed 
out into cavities filled with cheesy matter and pus. 

Sometimes the process comes to a standstill, and then the cheesy 
portions are infiltrated with the salts of lime. 

EMBOLISM AND THROMBOSIS. 

Acute and chronic endocarditis affecting the left side of the heart, 
and chronic endarteritis of the aorta, frequently result in the formation 
of vegetations, portions of which become detached and lodged as emboli 
in the branches of the renal artery. 

The occlusion of an artery in this way produces in the kidneys wedge- 
shaped infarctions, varying in their size with the size of the obstructed 
artery. The infarction loses the natural red color of the kidney, and 
becomes first yellow and then white. The renal epithelium degenerates 
and disappears, the tubes become collapsed and shrunken; around the 
infarction is a zone of congestion and of infiltration with pus cells. After 
this the infarction becomes shrunken, dense, and changed into connec- 
tive tissue. The kidney is then left deformed by the cicatricial depres- 
sions and contractions. It is possible, however, for the infarction to 
become gangrenous, or to be surrounded by a zone of purulent infiltra- 



416 THE URINARY APPARATUS. 

tion, and break down so as to form an abscess. Rarely the infarctions 
are of the hemorrhagic variety. 

Embolism of the trnnk of the renal artery produces complete necrosis 
of the kidney. 

Infectious emboli are small, and produce little purulent foci (see 
above). 

Thrombosis of the renal vein and its branches may occur in patients 
suffering from chronic Bright's disease. 1 It can also be produced by 
tumors pressing on the veins, by thrombi of the vena cava; and occurs 
as a primary lesion dependent on the general condition of the patient. 

HYDRONEPHROSIS. 

Dilatation of the pelvis and calyces of the kidney is found as a con- 
genital condition. In some cases, other malformations, such as club-foot, 
hare-lip, and imperforate anus, are also present. The pelves and calyces 
of both kidneys and the ureters are distended with urine; the bladder is 
also distended and its wall may be hypertrophied. The urethra may be 
closed, or no obstruction can be demonstrated. In these latter cases, it 
is supposed that there does exist some membranous obstruction, which is 
broken by the probe or catheter used to explore the urethra. 

In adult life, hydronephrosis is produced by mechanical obstruction 
of the urethra or ureters, due to inflammation, tumors, or calculi. Ac- 
cording to the position of the obstruction, either one or both kidneys are 
involved. 

The pelvis and calyces are dilated, sometimes enormously, and rilled 
with urine alone, or urine mixed with pus. The kidney tissue is flat- 
tened and thinned over the distended cavities. Its texture may remain 
unchanged, or there may be developed suppurative pyelo-nephritis or 
chronic diffuse nephritis. 

THE CYSTIC KIDNEY. 

Cysts are formed in the kidneys, both during intra-uteririe and extra- 
uterine life. 

The congenital cystic kidney is a very remarkable pathological con- 
dition. Either one or both kidneys are enormously enlarged and con- 
verted into a mass of cysts. The cysts are of all sizes and are separated 
from each other by fibrous septa or compressed kidney tissue. They 
contain a clear, yellow, acid fluid, holding in solution the urinary salts. 
Or the fluid is turbid and brown, and contains blood, uric acid crystals, 
and cholestearin. The cysts are lined with a single layer of flat poly- 
gonal cells. They seem to be formed by a dilatation of the tubules and 

1 Moxon, Trans. Lond. Path. Society, 1870, p. 248. 



THE URINARY APPARATUS. 417 

of the capsules of the Malpighian bodies. As causes for such dilatations 
are found obliteration of the tubes in the papillae, and stenosis of the 
pelvis, ureters, bladder, or urethra. Other congenital malformations 
are often associated with this one. 1 

In adult life we find three varieties of cystic kidney: 

1. In kidneys which are otherwise normal, there are one or more 
cysts filled with clear or brown serum or colloid matter. These cysts 
do not appear to interfere at all with the function of the kidneys. 

2. In chronic diffuse nephritis, especially in the atrophic form, groups 
of tubes are dilated. Apparently one or more of the larger tubes in the 
pyramids is obstructed, and this causes dilatation of a corresponding 
group of tubes. Such a dilatation may be moderate in size, or it may 
form cysts visible to the naked eye. 

3. Both kidneys are very much enlarged and converted into a mass 
of cysts containing clear or colored serum or colloid matter. The na- 
ture of these cysts is uncertain. It is possible that they are congenital. 
They are sometimes associated with similar cysts in the liver. They 
seem to produce no renal symptoms until shortly before the patient's 
death, unless chronic nephritis also exists, and then there are the ordi- 
nary symptoms of chronic Bright's disease. 

PERINEPHRITIS. 

. The loose connective tissue which is situated around and beneath the 
kidney may become the seat of suppurative inflammation, and in this 
way abscesses of considerable size are formed. 

Such a perinephritis may be either secondary or primary. The sec- 
ondary cases are due to extension of the inflammation from abscesses in 
the vicinity, such as are formed with caries of the spine, pelvic cellulitis, 
puerperal parametritis, perityphlitis, and suppurative nephritis. 

The primary cases occur after exposure to cold, after contusions over 
the lumbar region, and after great muscular exertion; or no cause can 
be discovered. 

Complicating cases occur in the coarse of typhus and typhoid fevers 
and of small-pox. 

Most of the reported cases have been in persons between the ages of 
twenty and forty years. Less frequently children and older persons are 
affected. 

* In the idiopathic cases, the connective tissue behind the kidney seems 
to be the point of origin of the inflammatory process, and it is here that 
the pus first collects. After the abscess has formed, the suppuration ex- 
tends and the pus burrows in different directions: backward through the 
muscles; downward into the iliac fossa, the perineum, the bladder, the 

^irch., Ges. Abhandl. 



418 THE URINARY APPARATUS. 

scrotum, or the vagina; forward into the peritoneal cavity or the colon; 
upward through the diaphragm. 

The kidney itself is simply compressed by the abscess, op its tissue 
becomes involved in the suppurative inflammation. 

RENTAL CALCULI. 

In the kidneys of new-born children, from the first to the fourteenth 
day after birth, the large tubes of the pyramids often contain small, 
brownish, rounded bodies composed of the urates of ammonium and 
sodium. Similar masses may also be present in the calyces and pelves. 
In still-born children these masses are usually absent. The carbonate 
and phosphate of lime may be deposited in the tubes of the pyramids, in 
the form of white linear masses, in the kidneys of old persons and of 
those who have suffered from destructive diseases of the bones. 

Urate of soda in the form of acicular crystals is deposited both in the 
tubes and stroma of the kidneys of gouty persons. 

Concretions of the urinary salts are often formed in the pelves of the 
kidneys. They may remain there as rounded masses, or they may attain 
a large size and be moulded into the shape of the pelvis and calyces. 
Smaller calculi may pass into the ureter and either become impacted 
there or pass through it into the bladder. The most common form of 
calculus is that composed of uric acid. But they may also be formed of 
uric acid with a shell of oxalate of lime, or of oxalate of lime alone, 
or of the phosphates, or of cystin. 

The most serious result of the presence of these calculi is the occlu- 
sion of the ureters or the production of pyelo-nephritis. 

TUMORS. 

Fibroma.— Small, hard, white fibrous nodules are frequently found 
in the pyramids. They are of no special importance. They may be 
mistaken for miliary tubercles. Large fibromata are very rare. 1 

Lipoma. — Small fatty tumors are found in the cortex of the kidney 
just beneath the capsule. They are composed of fully developed fat 
tissue. The fat is developed in the stroma so as to replace the kidney 
tissue. 2 

Papilloma. — Villous tumors formed of tufts of connective tissue cov- 
ered with epithelium may grow from the mucous membrane of the pel- 
vis. 3 A peculiar form of papillary and cystic growth of the ureter is 
described. 4 

1 Wilks, Trans. Lond. Path. Soc, xx. 

2 Virchoic, " Krank. Geschwulste," Bd. 1, p. 385. 

3 Trans. Lond. Path. Soc, 1870, p. 239. 

4 Virch. Arch., Bd. 66, p. 139. 






THE URINARY APPARATUS. 419 

My xo- Sarcoma. — Large tumors may grow from the pelvis of the 
kidney. They are not simple myxomata, but are composed of mucous 
tissue, fat, and sarcomatous tissue. 

Myoma. — Small tumors composed of smooth muscular fibres and of 
round cells are found in the cortex close to the capsule. 

A tumor composed of striated muscle and round cells is described by 
Oohnheim. 1 

A tumor composed partly of smooth muscle, partly of striped muscle, 
and partly of sarcomatous tissue, is described by Eberth. 2 

Angioma cavernosum occurs in the form of small nodules situated in 
the cortex. 

Lymphoma. — Small white tumors composed of tissue like that of the 
lymphatic glands are found in cases of leukaemia and pseudo-leukaemia. 
Less frequently they are found with typhoid fever, scarlet fever, and 
diphtheria. 

Adenoma. — This form of tumor is situated in the cortex of the kid- 
ney, and may invade the pyramidal portion also. Usually there is only 
a single tumor, but sometimes two or more, or they may even occur in 
both kidneys. They vary in size; some are not larger than a pea, others 
are as large as a hen's egg. They are of rounded form, of whitish color, 
and separated by a capsule from the kidney tissue. The tumors are 
most frequent in persons over forty years of age. 

There are two principal varieties of these tumors, the papillary and 
the alveolar. 

1. The Papillary Adenoma — There are cavities of different sizes, 
from the walls of which spring branching tufts covered with cylindrical 
or cuboidal epithelium. These tufts nearly till the cavities. 

.2. The Alveolar Adenoma. — There is a connective-tissue framework 
inclosing small round, oval, or tubular alveoli, lined or filled with cells. 
The cells are large, polygonal, nucleated bodies. 

The adenomata frequently undergo fatty degeneration, which may be 
•so complete that they look like fatty tumors. 

Or there may be an excessive development of the stroma, with atro- 
phy of the epithelial cells. 

There may be an excessive development and dilatation of the capilla- 
ries and veins in the stroma. 

Cysts of considerable size may be formed by dilatation of the cavities 
or alveoli. 3 

There are larger tumors involving the whole of the kidney, and ac- 
companied with metastatic growths in other parts of the body, which 
have the same structure as the papillary adenomata. 

1 Virch. Arch., Bd. 65, p. 64. 

* Virch. Arch., Bd. 55, p. 518. 

3 Medizinisch. Jahrb., 1883, p. 213. Virch. Arch., Bd. 93, p. 39. 



420 THE URINARY APPARATUS. 

A congenital adenoma is described by Weigert. 1 

Carcinoma. — Besides secondary carcinoma of the kidney, there is 
also a primary form. Our knowledge of this has "been much obscured, 
by confounding with it adenomata and sarcomata. 

There seems to be, however, a real epithelial growth, originating in 
the kidney tubules, which forms tumors of large size and malignant 
character. 

Sarcoma. — Tumors formed of conuective-tissue cells may originate 
either in the pelvis of the kidney or in the kidney itself. They form 
tumors of large size and malignant character. Those which grow from 
the 'pelvis are usually myxo-sarcomata. Those which originate in the 
kidney tissue reach a large size and are soft and hemorrhagic. Their 
stroma forms irregular alveoli filled with small round cells. 

PARASITES. 

Echinococcus, in its ordinary form of mother and daughter cysts, is 
sometimes found in the kidney. The cysts may open into the pelvis of 
the kidney, into the pleura, or through the wall of the abdomen. 

Cysticercus cellulosm is of very rare occurrence. 

Pentastomum denticulatum has been seen once by E. Wagner. 

Filaria sanguinis hominis is found in the arteries, veins, lymphatics, 
and stroma. 

Strongylus gigas has been found several times in the pelvis of the 
kidney. 

THE URINARY BLADDER. 

MALFORMATIONS. 

Extroversion of the bladder is one of the most frequent malforma- 
tions, and may occur in either sex. It presents several varieties: 

1. The umbilicus is lower down than usual, the pubic bones are not 
united at the symphysis, the pelvis is wider and shallower than it should 
be. Between the umbilicus and pubes the abdominal wall is wanting. 
In its place is a projecting, ovoid mass of mucous membrane, in which 
may be seen the openings of the ureters. The penis is usually rudimen- 
tary; the nrethra is an open fissure (epispadia); the clitoris may be sepa- 
rated into two halves. The ureters usually open normally; sometimes 
their openings are displaced or are multiple. They may be dilated. 

2. There may be a fissure in the abdominal wall, filled up by the 
perfectly -formed bladder. 

3. The umbilicus may be well formed, and there is a portion of ab- 
dominal wall between it and the extrophied bladder. 

4. The external genitals and urethra may be well formed, and the 
symphysis pubis united, while only the bladder is fissured. 

1 Yirch. Arch., Bd. 67, p. 492. 



the: urinary apparatus. 421 

5. The genitals, urethra, and symphysis may be well formed, the 
bladder closed except at the upper part of its anterior wall. The blad- 
der is entirely or in part inverted and pushed through the opening in the 
abdominal wall. 

The Urachus normally remains as a very small canal, five to seven 
cm. long, with a small opening into the bladder, or entirely closed at 
that point. If there is a congenital obstruction to the flow of urine 
through the urethra, the urachus may remain open and the urine pass 
through it. 

Absence of the Bladder is of rare occurrence. The bladder may be 
very small, the urine passing almost directly into the urethra. The 
bladder may be separated into an upper and a lower portion by a circular 
constriction. It may be completely divided by a vertical septum into 
two lateral portions. Diverticula of the wall of the bladder are some- 
times found in new-born children. Partial or complete closure of the 
neck of the bladder may occur. This may lead to hydronephrosis, or the 
urine may be discharged through the open urachus. 

CHANGES IN SIZE AND POSITION. 

Dilatation. — This may be general ov partial, leading to the formation 
of diverticula. 

General dilatation of the bladder is produced by the accumulation 
of urine in consequence of some mechanical obstacle to its escape, or of 
paralysis of the muscular walls of the organ. The dilatation is usually 
uniform and may be very great, so that the bladder may reach to the 
umbilicus. If the walls of the bladder are paralyzed, or the obstruc- 
tion occurs suddenly or is complete, the wall of the bladder is thinned. 
When an incomplete obstruction exists for some time, the walls of the 
bladder are apt to hypertrophy, so that, although the bladder is larger 
than normal, the walls may not only be of the usual thickness, but even 
very much thicker. In the foetus, dilatation of the bladder may reach 
such a size as to interfere with delivery. 

The retained urine in dilated bladders is liable to decomposition, 
leading to inflammation or gangrene of the mucous membrane. 

Diverticula of the bladder may be produced by the pouching-out of 
circumscribed portions of the wall of the bladder, the wall of the pouch 
containing all the layers of the bladder wall. More frequently, however, 
they are produced by a protrusion of the mucous membrane between 
hypertrophied bundles of muscle fibres. They may be very small, or 
they may be as large as a child's head. They may communicate with 
the bladder by a large or a small opening. The decomposition of stag- 
nant urine in diverticula is apt to induce inflammation. Calculi may be 
formed in them or may slip into them from the bladder. 

Hypertrophy of the muscular coat of the bladder is usually produced 



422 THE URINARY APPARATUS. 

by mechanical obstructions to the outflow of urine, such as stricture of 
the urethra, enlarged prostate, calculi, new growths, etc. The muscular 
coat is thickened uniformly or assumes a trabeculated appearance. The 
organ retains its normal capacity, or is dilated, or becomes smaller. The 
mucous membrane is frequently the seat of chronic or acute inflamma- 
tion. Dilatation of the ureters and hydronephrosis frequently accompany 
this condition. 

Hernim of 'the bladder sometimes accompany intestinal hernias 
through the inguinal and crural canals and the foramen ovale. The 
changes in position of the bladder, produced by displacements of the 
vagina and uterus, will be mentioned with the lesions of those organs. 

In the female, the base of the bladder may press downward, causing 
protrusion of the vaginal wall (vaginal cystocele); or there maybe inver- 
sion and prolapse of bladder through the dilated urethra. 

RUPTURE — PERFORATION". 

Penetrating wounds of the bladder may permit escape of urine into 
the abdominal cavity, or infiltration into the surrounding connective 
tissue, or permanent fistulas. Such wounds are always serious and fre- 
quently fatal, owing chiefly to the severe and often gangrenous inflam- 
mation which decomposing urine sets up in the connective tissue, or to 
the peritonitis induced by the same cause. 

Rupture of the bladder may be produced by severe blows and falls 
when the bladder contains urine. More rarely, rupture takes place from 
over-distention. Death may occur from rupture of the bladder with 
escape of urine into the peritoneal cavity, without evidences of peritonitis. 

Perforations of the bladder are produced by ulceration and gangrene, 
by abscesses from without, and by cancerous ulceration from the adjoin- 
ing organs. Fractures of the pelvic bones may produce laceration of the 
bladder. Perforations of the bladder may lead to the establishment of 
fistulas, communicating with the rectum, vagina, uterus, or opening 
externally. 

DISTURBANCES OF CIRCULATION. 

Hyperemia. — Aside from active hyperemia of the mucous membrane 
in acute inflammation, the bladder is not infrequently the seat of chronic 
congestion from obstruction to the venous circulation. Under these 
conditions, there may be chronic catarrhal inflammation, or a marked 
dilatation of the veins (vesical haemorrhoids), which may give rise to 
haemorrhage, or to obstruction of the opening of the ureters. 

Hemorrhage. — Extensive haemorrhages into the bladder are com- 
monly due to injury or to the presence of calculi or tumors. Small 
haemorrhages into the substance of the mucous membrane may accom- 
pany inflammation, the haemorrhagic diathesis, scurvy, purpura, small- 



THE URINARY APPARATUS. 423 

pox, etc. If the haemorrhage is considerable and occurs rapidly in an 
empty bladder, a clot is apt to form; but when the blood mixes with 
urine as it is extravasated, it more commonly remains liquid and is dis- 
charged as a reddish-brown fluid. 

INFLAMMATION. 

Acute Catarrhal Cystitis. — This may be incited by the presence of 
urine which has decomposed under the influence of bacteria; by can- 
tharides or other drugs; by the presence of foreign bodies and calculi; 
or it may be due to an extension of gonorrheal urethritis or vaginitis; or 
it may occur without assignable cause. The mucous membrane is swol- 
len and congested, although these alterations may not be very evident 
after death. The surfaces may be coated with mucus containing red 
blood-cells and pus. The epithelium is apt to be loosened and in some 
places peeled off, so that superficial or deep ulceration may occur. We 
may find mixed with the urine in the organ shreds of mucus, pus cells, 
epithelial cells of various shapes, usually more or less swollen and granu- 
lar, or fragments of such cells; red blood-cells and bacteria. Resolu- 
tion may occur from acute catarrhal cystitis, but it very frequently 
assumes a chronic character. 

Chronic Cystitis. — In this form the mucous membrane may be swol- 
len, succulent, grayish, or mottled with spots of congestion or extravasa- 
tion, and covered with a layer of mucus and pus. Microscopically the 
membrane may be more or less infiltrated with pus cells, and pus may be 
constantly produced and thrown off into the urine. Later the mucous 
membrane may become thickened either diffusely or in the form of tufts 
or polypi. In some cases it becomes atrophied. Owing to decomposi- 
tion of the haemoglobin in the extravasated blood, the mucosa may be- 
come pigmented, brown, or slate-colored. The mucous membrane fre- 
quently becomes eroded, especially on the most elevated portions, or 
deep ulcerations may occur. The muscular coats may become paralyzed 
and the bladder dilated; or the submucosa or the muscularis, or both, 
may become hypertrophied. The mucous membrane may become in- 
crusted with urinary salts. 

In another class of cases, the inflammation assumes a more intense 
and necrotic character. Larger and smaller shreds and patches of 
the mucosa die, become brown or gray in color, loosen or peel off, and 
become mixed with the urine and exudations. The gangrenous process 
may extend to all the coats of the bladder, so that perforation and fatal 
peritonitis may occur. The gangrenous form of cystitis is most apt to 
occur in paralytics. In still another class of cases, the inflammation 
assumes a suppurative character. The submucosa, the intermuscular 
connective tissue, and the adjacent parts become infiltrated with pus, 
either diffusely or in the form of larger and smaller abscesses, which 



424 THE URINARY APPARATUS. 

may open externally or internally, forming deep ulcers. In all these 
cases the inflammation may extend to the ureters and kidneys; it may 
skip the ureters and involve the kidneys. 

Croupous Inflammation. — In connection with any of above lesions, 
the mucous membrane of the bladder may be covered, in patches or some- 
times over a considerable portion of its surface, with a layer of fibrin, 
either granular or fibrillar, inclosing pus and epithelial cells and bac- 
teria. The mucosa may be infiltrated with fibrin. 

This form of inflammation may occur in connection with severe in- 
fectious diseases — measles, diphtheria, scarlatina, typhoid fever; in con- 
nection with similar inflammation of the external genitals, in puerperal 
fever, noma, and sometimes in the presence of foreign bodies. It is 
rarely an idiopathic disease. 

Tubercular Inflammation. — This disease commences by the formation 
of miliary tubercles in the mucous membrane of the bladder. By the 
coalescence of the tubercles and the degeneration of tissue about them, 
ulcers are formed, and it is most frequently in the ulcerative stage that 
the lesion is seen. The ulcers, which may be large or small, are usually 
most abundant at the base of the organ. Their edges may be cheesy, 
and miliary tubercles in greater or smaller numbers are usually found in 
the mucosa about them. Not infrequently large shreds of tissue are 
loosened and cast off. The mucosa about the ulcers is apt to be infil- 
trated with small spheroidal cells. Tubercle bacilli are present in many 
of the tubercles, and in the edges and base of the ulcers. They may 
also be found in the urine, and are then of diagnostic significance. 
Catarrhal inflammation is a very constant accompaniment of. this lesion. 
Tubercular cystitis may occur in connection with tubercular inflamma- 
tion of the lungs, intestines, or of the kidney, uterus, prostate, etc. 

TUMOKS. 

Fibromata have been described, occurring as small nodular tumors in 
the submucosa, but they are rare. 

Aside from the polypoid thickenings of the mucosa occurring in 
chronic cystitis, soft vascular papillomata are of frequent occurrence. 
These tumors vary in size from that of a pea to that of a pigeon's egg 
or larger. They consist of a fibrous, often very vascular stroma, and are 
covered on the surface with numerous small, closely set, villous projec- 
tions, over which are irregular layers of elongated or cylindrical cells. 
These tumors are very liable to bleed, are often accompanied by vesical 
catarrh, and may be covered by a precipitate of urinary salts. The epi- 
thelium is liable to peel off from the surface of the villi and appear in 
the urine. Sarcoma of the bladder has been described. 

Carcinoma. — Carcimonaof the bladder is most frequently secondary, 



THE URINARY APPARATUS. 425 

and is then rarely due to metastasis, but usually to an extension of the 
growth from neighboring parts, as the uterus, vagina, or rectum. 
Primary carcinoma of the bladder may occur : 

1. As a diffuse scirrhous infiltration of the entire wall of the blad-. 
der, usually with ulcerations of its inner surface. 

2. As a circumscribed nodule which grows inward aud outward, ul- 
cerating on its inner surface, and sometimes producing perforations. 

3. As villous or papillomatous growth. The tumor grows from one 
or more points of the inner surface of the bladder. It is formed of tu- 
bular follicles lined with cylindrical epithelium, and, on its inner free 
surface, of tufts covered with cylindrical epithelium. The new growth 
may involve the entire thickness of the wall of the bladder. 

4. A few cases of carcinoma have been described in which the stroma 
contained a varying quantity of smooth muscle tissue. 1 

Cysts. — Dermoid cysts of the wall of the bladder have been described, 
but are rare. Small cysts with serous contents sometimes occur in the 
mucous membrane. A part of them, at least, are believed to be due to 
faulty embryonal development. 

PARASITES, ETC. 

Among the animal parasites occasionally found in the bladder may 
be mentioned Echinococcus, Distoma haematobium, Filaria sanguinis, 
Ascarides, and Oxyurides. 

Bacteria of various forms not infrequently occur in the bladder, par- 
ticularly in connection with chronic cystitis. B. termo, Micrococcus 
ureal, and Sarcina may be mentioned as of most frequent occurrence. 

A great variety of foreign bodies may be found in the bladder, par- 
ticularly in the female. If their stay is long, they are apt to become in- 
crusted with urinary salts. 

CALCULI. 

Vesical calculi may occur singly or in great numbers, and vary greatly 
in size, ranging from small, sand-like particles up to masses four or five 
inches in diameter, but the usual range is from the size of a pea to that 
of a hen's egg. They are usually oval, spheroidal, or elongated; or, 
when several are present, they are apt to be faceted. The surface may 
be smooth or rough. They are usually more or less distinctly lamellated, 
and are frequently formed around a central body called a nucleus, which 
may either be formed of urinary salts or some foreign body. Their most 
common constituents are phosphates, uric acid and urates, and calcium 
oxalate, or various combinations of these. 

Uric Acid Calculi. — These are the most common of vesical calculi. 

1 The literature of tumors of the bladder may be found in Stein's ' ' Study of the 
Tumors of the Bladder," 1881. 
33 



426 THE URINARY APPARATUS. 

In the form of small brownish-red, crystalline aggregations they may be 
passed as " gravel." The larger uric acid calculi are not commonly of 
very great size, are frequently finely nodulated on the surface, but may 
be smooth. The color varies from light yellow to dark reddish-brown; 
they are usually dense and lamellated. 

Calculi formed of Urates. — Calculi composed of pure urates are rare, 
these salts being more commonly combined with uric acid and the phos- 
phates to form the complex calculi. Sodium urate, in the form of small 
spined, more or less globular crystalline masses, forms one of the varie- 
ties of "gravel/' 

Phosphatic Calculi. — Pure calcium phosphate calculi are rarely found, 
as whitish, usually smooth, and small lamellated concretions. 

Mixed or Triple Phosphate calculi are common, and frequently attain 
large size. These calculi are sometimes pure, but the deposit is more 
frequently associated with other salts, either as incrustingor intercalated 
lamellae. Triple phosphate calculi are usually rough on the surface, of 
grayish-white color, lamellated. and frequently very friable. 

Small gray or white, hard, and usually smooth calculi of pure calcium 
carhonate occur rarely. Calcium carbonate is sometimes passed as gravel 
in the form of minute spheroidal bodies, either singly or in clusters. 

Calcium Oxalate calculi (mulberry calculi) are comparatively com- 
mon, either pure or in combination with uric acid or the phosphates. 
Calcium oxalate may occur in the form of very small, hard, smooth con- 
cretions, or as larger, heavy, hard, finely or coarsely nodulated brown or 
blackish lamellated masses. The nucleus or some of the lamellaB, or 
both, are often composed of uric acid. 

Cystin Calculi are usually ovoidal in shape, of waxy consistence, of 
clear or brownish or greenish-yellow color, with mammillated surface and 
crystalline fracture. Cystin may be associated in a variety of ways with 
other calculi. 

Xanthin Calculi, which are very rare, are usually of moderate size, 
smooth, of a cinnamon or cinnabar-red color, lamellated, and oval or 
flattened in shape. 

Solid masses of fibrin and blood sometimes occur in the bladder, and 
may exist as independent structures, or form nuclei for the deposit of 
urinary salts. 

For a detailed account of calculi, the conditions under which they 
form, modes of analysis, etc., we refer to special works on this subject. 



THE URINARV APPARATUS. 427 



THE URETHRA. 



CONGENITAL MALFORMATIONS. 

Some of the malformations of the urethra are described with those of 
the penis. 

The urethra may be impervious, or may open at the root of the penis. 
More commonly there is partial obliteration or stricture of some part of 
the canal. 

The entire urethra may be dilated into a sac full of urine. 

There may be a canal on the dorsum of the penis, formed by the 
fusion of the spermatic cords, and opening in the glans above the 
urethra. 

There may be two or more openings of the urethra. 

The canal may be dislocated so as to open in the inguinal region. 

A number of cases have been reported in which a valve in the urethra 
has produced hypertrophy of the bladder, dilatation of the ureters, and 
hydronephrosis. 1 

Owing to its narrowness, greater length, and peculiar connections 
with the internal generative organs, the male urethra is much more 
liable to disease than the female. 

CHANGES IN SIZE AND POSITION. 

Dilatation of the urethra may be produced by strictures, or by calculi 
or other bodies fixed in its lumen. The dilatations are fusiform or sac- 
culated in shape, and may reach the size of an orange or be even larger. 

Strictures of the urethra are usually produced by inflammation of its 
walls. 

The stricture may be temporary, produced by a diffuse inflammatory 
sweliiog of the mucous membrane, or by the raising of the relaxed mem- 
brane into a fold or pocket. 

Permanent strictures are produced by structural changes in the walls 
of the urethra. 

1. The mucous membrane and submucous tissue are left hard and 
unyielding by the preceding inflammation. Subsequently the new 
fibrous tissue contracts and narrows the canal. 

2. Ulceration of the mucous membrane leaves cicatricial tissue, which 
contracts, and also produces adhesions and bands of fibrous tissue. 

3. There is fibrous induration of the corpus spongiosum, and conse- 
quent constriction of the urethra. 

The most frequent position of strictures is at the junction of the 
membranous and spongy portions of the urethra, or close to this point. 

1 Virch. Arch., Bd. 49, p. 348. 



428 THE URINARY APPARATUS. 

They also occur at the fossa navicularis and the meatus, but frequently 
in the prostatic portion. There may be one stricture or several. The 
consequences of stricture are dilatation of the urethra, the bladder, the 
ureters, and hydronephrosis; inflammation and ulceration of the urethra 
behind the stricture, with perforation, infiltration of urine, or the for- 
mation of fistulse. 1 

The urethra may also be obstructed by folds of the mucous membrane; 
by muscular valves, at the neck of the bladder; by wounds; by polypi 
and swollen glands; by new growths; by changes in the prostate and 
perineum; by calculi, mucus, blood, and echinococci coming from the 
bladder; by foreign bodies introduced from without. 

Prolapse and inversion of the mucous membrane is seen in young 
girls and women in rare cases. There is a bluish-red swelling, from the 
size of a pea to that of a walnut, at the meatus. In the male, invagina- 
tion of the mucous membrane of the urethra has been seen after injuries 
of the perineum. 

WOUNDS— RUPTURE — PERFORATION. 

Wounds of the urethra are produced in many ways, but most com- 
monly by catheters and bougies. The wounds may cicatrize, or there 
may be infiltration of urine or the formation of fistulae or false passages. 

Ruptures of the urethra are produced by severe contusions and by 
fracture of the pelvic bones. Extravasations of blood and urine, and 
gangrenous inflammation of the surrounding soft parts, are the ordinary 
results. 

Ulceration and perforation of the urethra may lead to the formation 
of fistulae, which open in various directions through the skin. 

INFLAMMATION. 

Catarrhal Urethritis may be simple and due to the action of chemi- 
cal irritants, to the extension to the urethra of inflammation from other 
parts, and to unknown causes; but it is most frequently due to the action 
of the gonorrhoeal poison. In its acute form it involves either a portion 
or the whole of the urethra. The mucous membrane is red, swollen, and 
covered with muco-pus. The inflammation may extend to the fibrous 
wall of the urethra, the corpora spongiosa and cavernosa. This may re- 
sult in the formation of new connective tissue or of abscesses, especially 
near the fossa navicularis. The inflammation may also extend to the 
bladder, the glands of Oowper, the prostate, the spermatic cord, and the 
testicles. The inguinal glands also may be swollen and inflamed, and 

1 For literature of stricture of urethra and plates illustrating several forms, see 
article by Dittel in Pitha and Billroth's " Handbuch der allg. Chirurgie," Bd. 3, 
Abth. 3. 






THE URINARY APPARATUS. 429 

the lymphatic vessels on the dorsum of the penis may be involved in the 
same process. 

Chronic inflammation of the urethra may exist for a long time with 
the production of a muco-purulent exudation, but without the occur- 
rence of marked structural lesions. In other cases it leads to ulceration, 
to fibrous induration of the wall of the canal, to induration and swelling 
of the mucous follicles, to polypoid thickenings of the mucous mem- 
brane. 

The exudation in gonorrheal inflammation of the mucous mem- 
branes, not only of the urethra but also of the vagina and of the eye, 
constantly contains, in greater or less numbers, a form of micrococcus 
which is said by some observers— although this is denied by others — to 
present characteristic morphological characters. 

The micrococcus— called gonococcus — which is spheroidal or ovoidal 









iir 



Fig. 184.— Gonococci contained in Pus Cells. 
From a case of gonorrhceal urethritis. 

in shape, usually occurs in pairs or in groups of four or more, and may 
be contained in the pus cells (Fig. 184) or lie on their surfaces or free 
in the fluid. The pus cells sometimes contain very large numbers of the 
micrococci. While the very constant presence of these micrococci justi- 
fies the conjecture that they may stand in an etiological relation to the 
gonorrhceal inflammation, the experiments thus far recorded upon their 
purification by culture and inoculation have not led to such definite re- 
sults as to justify us in assigning to them a definite role in the disease. 
The conclusions of investigators are in many respects at variance; the 
results of animal inoculations are usually negative, and the inoculations 
thus far practised on the human subject have not been sufficiently ex- 
tensive and exact. 

The gonococcus may be stained by drying the exudation on a cover 
glass and using fuchsin or methylin blue. 



430 



THE URINARY APPARATUS. 



Croupous Inflammation is sometimes seen in children. Fibrinous 
casts of a small or large portion of the canal may be formed. 

Syphilitic Ulcers may be situated at the meatus or as far back as the 
fossa navicularis. They are apt to produce strictures. 

Tubercular Inflammation rarely occurs in the mucous membrane of 
the urethra in connection with tubercular inflammation of the bladder, 
prostate, or testicles. 

TUMORS. 

Aside from the polypoid outgrowths from the mucous membrane of 
the urethra as the result of chronic inflammation, fibrous polyps may 
occur congenitally, or polyps containing glandular structures or cysts 
rarely occur. Carcinoma may occur as a result of local extension from 
adjacent organs or metastasis from the bladder. Cysts may occur in the 
mucous membrane as a result of the dilatation of the mucous glands. 
Circumscribed, masses of dilated veins occasionally occur in the urethra, 
forming the so-called urethral haemorrhoids. 

The sinus pocularis may be dilated in children by the retention of its 
secretion, so as to form a tumor which may obstruct the exit of urine, 
cause hypertrophy of the bladder and dilatation of the ureters. 



THE ORGANS OF GENERATION. 



FEMALE. 

THE YULVA. 

MALFORMATIONS. 



The external genitals may be entirely absent or imperfectly developed. 
The fissure between the labia may be unformed, or the labia may grow 
together, with or without obstruction of the urethra. The clitoris and 
nymphse may be abnormally large or the nymphae may be increased in 
number. The clitoris may be abnormally long, resembling a penis; at 
the same time the vagina is narrow, the uterus small and undeveloped 
or malformed; the ovaries small, sometimes situated in the labia; the 
mammas small, and the body of a masculine character. Such cases are 
sometimes called pseudo-hermaphrodites. The clitoris may be perforated 
by the urethra, or may be cleft and apparently double. 

The hymen frequently exhibits various anomalies. It may be en- 
tirely absent. The opening may be very large or in unusual places; 
there may be several openings; the free edge may be beset with papillary 
projections; there may be no opening at all. 1 

HEMORRHAGE, HYPEREMIA, ETC. 

Haemorrhage may take place from wounds or ulcers of the vulva, but 
the most important form of hasmorrhage is that which occurs in the con- 
nective tissue of the labia majora This is produced during labor or 
from external injury. One of the labia may be swollen and distended by 
the extravasated blood until it is as large as a child's head. The blood 
may be gradually absorbed, or it may decompose with suppuration or 
gangrene of the surrounding tissue. The purulent matter may escape 
through the skin and the patient recover, or the suppuration may ex- 
tend into the pelvis and cause death. 

A varicose condition of the veins of the labia is not infrequent. 

1 For description and illustrations of anomalies of the hymen, which may be useful 
for medico-legal purposes, see Courty's " Diseases of Uterus, Ovaries, Fallopian 
Tubes," Trans, by McLaren, 1883, p. 90. 



432 THE ORGANS OF GENERATION. 

(Edema may occur in acute form in pregnant and puerperal women, and 
may terminate in suppuration or gangrene. (Edema of the labia majora 
frequently accompanies disturbances of the venous circulation, as in cer- 
tain heart and lung diseases; or it may occur in chronic diffuse nephritis 
or other wasting diseases, or as a result of thrombosis or other distur- 
bances of circulation in the uterine or perivaginal venous plexuses. 
This may be excessive, leading to the transudation of fluid through the 
skin, to the formation of vesicles, to superficial erosion, or even to gan- 
grene. 

INFLAMMATION. 

The skin, mucous membrane, connective tissue, and glands of the 
vulva may be the seat of inflammation. Acute catarrh of the mucous 
membrane may be caused by a variety of irritating influences, but is most 
frequently due to gonorrheal infection. The mucous membrane is 
swollen and red and covered with a muco-purulent exudation. The 
labia may be swollen, and the glands are liable to be involved, and ab- 
scesses of the labia may be developed. Chronic catarrhal inflammation 
may lead to superficial or deep ulceration of the mucous membrane, or to 
papillary outgrowths, or to thickening of the labia. Suppurative in- 
flammation of the tissue of the labia may occur in connection with a 
similar process in neighboring parts. Erysipelatous inflammation of the 
skin of the vulva is frequent in young children and may cause death. 
In adults it is less common. Inflammation of the vulvo-vaginal glands 
may be acute and produce abscesses, or chronic and produce induration 
of the gland. 

Gangrene may follow erysipelatous inflammation, may occur after 
parturition, may accompany severe exhausting and infectious diseases, or 
may occur as an epidemic disease, especially among children. It may be 
the result of bruises or other injuries. In some forms, such as those 
known as noma and hospital gangrene, the destruction of tissue proceeds 
with extreme rapidity. 

Herpes, eczema, lichen, prurigo, etc., may be found on the skin of 
the vulva. 

Syphilitic inflammation and ulceration are of frequent occurrence on 
the vulva, particularly on the mucous surfaces, and frequently lead to 
considerable destruction of tissue and cicatricial contractions. 

Croupous Inflammation may occur with or without diphtheria and a 
similar lesion of the fauces, and is frequently associated with gangrene. 

Lupus. — This form of inflammation, usually with more or less de- 
structive ulceration, occasionally occurs in the vulva. 

TUMORS. 

Fibroma. — Circumscribed fibrous tumors are found in the connective 
tissue of the labia, mons veneris, perineum, clitoris, and entrance to the 



THE ORGANS OF GENERATION. 433 

vagina. They may attain a large size, and, attached only by a pedicle, 
may hang far down between the legs. The skin is usually movable over 
the surface of these tumors. 

Fibroma diffusum (elephantiasis). — This usually involves the clitoris 
or the labia, or both, and may extend to surrounding parts of the skin. 
It consists essentially of a diffuse hypertrophy of the skin and subcuta- 
neous tissue, with or without involvement of the papillae and epidermis. 
The surface may be smooth or rough. Sometimes when the new growth 
is circumscribed, rough or smooth polypoid growths, often of large size, 
are formed. When the papillae and epidermis are much involved, 
larger and smaller cauliflower-like excrescences may cover the hypertro- 
phied parts, and the surface be very rough and scaly. 

Papillomata. — These growths consist of hypertrophied papillae covered 
with thick layers of epithelium. They vary in size from that of a pea to 
that of an apple, and have a cauliflower appearance. 

Syphilitic Condylomata. — In one form, the so-called mucous patch, 
there is an infiltration of the papillary layers of the skin or mucous mem- 
brane with variously shaped cells and fluid, so that the tissue has a gela- 
tinous appearance. In other cases, there is an hypertrophy of the pa- 
pillae, so that larger and smaller wart-like excrescences are formed. This 
is called the pointed condyloma. Lipomata, fibro-myomata, and fibro- 
sarcomata are of occasional occurrence in the vulva. A few cases of 
melano-sarcoma are recorded. Chondroma of the clitoris has been de- 
scribed. Carcinoma of the vulva may be primary, usually in the form 
of epithelioma of the clitoris or labia, or it may be secondary to cancer 
of the uterus, vagina, etc. 

Cysts are found in the connective tissue of the labia majora and 
minora. They are from the size of a pea to that of a child's head. 
They may contain serum, colloid material, purulent or bloody fluid, or 
they may have the. characters of dermoid cysts or atheroma cysts. Their 
origin is in many cases obscure. In some cases they are doubtless due 
to dilatation of lymph vessels. Cysts may be formed by a stoppage and 
filling with fluid of the canal of Nuck, or by a dilatation of the ducts or 
acini of the vulvo-vaginal glands. 



THE VAGINA. 

MALFORMATIONS. 

The vagina may be entirely absent, and the internal organs of gene- 
ration also absent or imperfectly developed. 

Either the upper or the lower portion of the canal may be absent 
while the remaining portion is present. 

The vagina may be closed by an imperforate hymen or by fibrous 
34 



434 THE ORGANS OF GENERATION. 

septa at any part of its canal. The canal may be abnormally small with- 
out being occluded. 

The vagina may be double, in connection with a double uterus; or, 
while the uterus is normal, the vagina may be incompletely divided by 
a longitudinal septum. 

CHANGES IN SIZE AND POSITION. 

Dilatation of the vagina is produced by tumors, by the prolapsed 
uterus, and by the accumulation of blood and mucus behind constric- 
tions or obliterations of the canal. Lengthening of the vagina is pro- 
duced by any cause which draws the uterus upward. Narroiving of the 
vagina is found as a senile change; is produced by tumors and by ulcera- 
tion of the wall of the canal. Extensive ulcers may even cause entire 
obliteration of the canal. 

Prolapse of the vagina occurs by itself, usually as a result of thicken- 
ing or laxity of its walls, or in connection with prolapse of the uterus. 
As an idiopathic process, it usually takes place soon after parturition. 
A larger or smaller portion of the canal is inverted and projects through 
the vulva. The entire circumference of the canal may be inverted and 
prolapsed, or only the anterior or posterior wall. The prolapse is at 
first small, but may afterwards gradually increase in size, and may drag 
down the uterus with it. In other cases, prolapse of the uterus is the 
primary lesion, and the vagina is inverted by the descent of that organ; 
or the body of the uterus may retain its normal position, while an hyper- 
trophy and lengthening of the cervix alone drag down the vagina. 

Hernia vesico-vaginalis — cystocele — may be either the cause or 
effect of a prolapse of the vagina and uterus. If the cystocele is the 
primary lesion, it begins as a small projection of the wall of the bladder 
into the anterior part of the vagina. As the urine accumulates in this 
sac, it increases in size, projects through the vulva, draws down the 
vagina and the anterior lip of the cervix, and finally the entire uterus. 
If the cystocele is the secondary lesion, it is. simply produced by the 
dragging-down of the posterior wall of the bladder by the inverted 
vagina. 

Hernia intestino-vaginalis. — A portion of the intestines may be- 
come fixed in Douglas' cul-de-sac between the rectum and uterus. This 
portion of intestine gradually becomes larger, pushes forward the pos- 
terior wall of the vagina, inverts and fills up that canal, and finally pro- 
jects through the vulva. It may drag with it the posterior wall of the 
vagina and the uterus. 

Rectocele vaginalis. — A sac is formed by the projection of the an- 
terior wall of the rectum and the posterior wall of the vagina. This 
lesion is of rare occurrence, and does not reach a large size. 



THE ORGANS OF GENERATION. 435 

When the vagina is prolapsed, there is usually an inflammatory con- 
dition of the lining membrane or a thickening of the epidermis. 

WOUNDS — PERFORATIONS. 

Wounds of the vagina are made by penetrating instruments, by for- 
ceps and other obstetrical weapons, and by the foetus during delivery. 
Such wounds may heal, may give rise to large haemorrhages, may suppu- 
rate, may produce abscesses in the surrounding tissues, may leave fistu- 
lous openings into the vagina, or may cause constriction or obliteration 
of its canal. 

Vesico-vaginal Fistula are usually produced by injuries from instru- 
ments or from the foetus during delivery; less frequently by ulceration 
of the vagina, bladder, or adjacent connective tissue, or by abscess in the 
surrounding parts. The fistulas form an opening between either the 
bladder or the urethra and the vagina. They allow the urine to pass into 
the vagina. Spontaneous cure does not take place. 

Recto-vaginal Fistula are formed in the same way as the last-men- 
tioned. They allow the passage of gas or faeces into the vagina. They 
sometimes heal spontaneously. 

INFLAMMATION. 

Catarrhal Inflammation of the vaginal mucous membrane may be 
acute or chronic. It is most frequently caused by gonorrhceal infection, 
but may be due to local irritation or depend upon general causes. It 
not infrequently occurs in the new-born. In the acute form, the mucous 
membrane is swollen and frequently covered with a muco-purulent or a 
purulent exudation. In the chronic form, the mucous membrane may 
be swollen, covered with a purulent exudation; there may be an exfolia- 
tion of epithelium, shallow or deep erosions, or ulcers. In other cases, 
the mucous membrane is thickened, dense, and sometimes pigmented,, 
or it may be roughened, covered with papillae, or it may be relaxed and 
prolapsed. 

Croupous Inflammation may occur after parturition, in dysentery, 
in typhus and typhoid fever, diphtheria, scarlatina, measles, and other 
infectious diseases. The mucous membrane is swollen and covered with 
a grayish layer of fibrin and pus. The mucosa and submucosa may be 
infiltrated with fibrin and pus. The infiltrated portions of the mucosa 
and submucosa may die and become gangrenous, and thus deep and ex- 
tensive ulcers be formed. 

Suppurative Inflammation of the fibro-muscular coat of the vagina 
may occur after injuries or in pregnant and puerperal women. Abscesses 
may be formed which penetrate into the labia or into the pelvic connec- 
tive tissue. In other cases, the intense phlegmonous inflammation may 



436 THE ORGANS OF GENERATION. 

lead to the death and casting-off of portions of the vaginal wall, or even 
of the entire wall. 

Gangrene of the vagina may occnr as a result of croupous or intense 
suppurative or syphilitic inflammation, or from unknown causes. In 
the form of noma it may be very extensive and rapidly destructive. 

Tubercular and Syphilitic Inflammation, usually leading to more or 
less extensive ulceration, may occur in any part of the vagina. Tuber- 
cular inflammation is secondary to tuberculosis of other parts. Syphilitic 
ulcers may heal, sometimes leaving marked cicatrices, and sometimes not. 

TUMORS. 

Fibroma, fibro -myoma, sarcoma, myoma laivicellulare, are of occa- 
sional occurrence in the vagina. Myoma strio cellular e is of rare occur- 
rence. 

Papillomata are of frequent occurrence as a result of chronic inflam- 
mation. Carcinoma of the vagina is usually secondary to cancer of the 
uterus. It may be primary as a circumscribed nodular tumor, or more 
frequently it occurs in a papillary and ulcerating form and often spreads 
to neighboring parts. 

Cysts. — These are not very common aud may be small or as large as 
a hen's egg. They may be lined with flattened epithelium, and contain 
serous or viscid, dark-colored or transparent fluid. 

PARASITES. 

Among the animal parasites, Oxyuris and Trichomonas vaginalis are 
of occasional occurrence. Among the vegetable forms Oidium albicans, 
Leptothrix are occasionally seen, while micrococci and various other 
forms of bacteria are common. The pathogenic significance of the bac- 
teria in the vagina is not yet established. 

THE UTERUS. 
MALFORMATIONS. 

The uterus, up to the third month of intra-uterine life, consists of 
two large cornua, which by the fusion of their lower ends form the 
uterus. 

The uterus, tubes, and vagina may be entirely absent, with or with- 
out absence of the external genitals. Or the uterus alone, or the upper 
part of the vagina also, may be absent. 

The uterus may be only rudimentary, while the vagina is normal. 
It then appears as a flattened solid body with solid cornua. Or there are 
two cornua joined at their lower extremities so as to form a small double 
uterus. Or the uterus is represented by a small sac, which may or may 



THE ORGANS OF GENERATION. 437 

not communicate with the vagina. Or there is a very small uterus, with 
thin muscular walls and two large cornua. 

Only one of the cornua which should form the uterus may be devel- 
oped, while the other is arrested in its growth. The uterus is then a 
long, cylindrical body, terminating above in one tube. On the side 
where the other horn should have been developed there is no tube, or 
only a rudimentary one. Both ovaries are usually present. 

The two cornua may be fully developed, but their lower ends remain 
separated and form a double uterus. An entire separation into two 
distinct uteri and vaginae is very rare. More frequently the uterus con- 
sists of one body, divided by a septum into two cavities. There are then 
two cervical portions of the uterus projecting into a single vagina, or 
each into a separate vagina. Or there is only a single cervix. The 
septum in the uterus may be complete or only partial. 

We also find abnormal size of the uterus, abnormal flexions; the cer- 
vix may be solid, or may be closed by the vaginal mucous membrane. 
Or the cervix may have an abnormal form with a small opening or 
canal. 1 

CHANGES IN SIZE. 

In the new-born infant, the uterus is small, the body flattened, the 
cervix disproportionately large. During childhood, the organ increases 
in size, but the body remains small in proportion to the cervix. At 
puberty the sha}3e changes and the body becomes larger. 

At every menstruation the uterus is somewhat swollen and congested. 
After pregnancy it does not return to its virgin size, but remains some- 
what larger. In old age, it gradually becomes smaller; its walls are 
harder and more fibrous. 

Abnormal Smallness of the uterus is sometimes found as an arrest of 
development. The uterus in adult life retains the size and shape of that 
of the infant. It may result, however, from chronic endometritis, from 
repeated pregnancies, from old age, or from chronic exhausting dis- 
eases. Its cavity may be smaller than normal, or distended with mucus. 
Large myomata sometimes cause marked atrophy of the uterine wall. 
Atrophy of the vaginal portion of the uterus is sometimes observed after 
repeated pregnancies, sometimes without known cause. Narrowing and 
obliteration of the cavity of the uterus and of the cervix are usually pro- 
duced by chronic inflammation. 

Enlargement of the Uterus may be due to too early development. It 
is accompanied by abnormally early development of all the sexual organs 
and functions. The uterus may be enlarged in connection with heart 
disease, prolapse and abnormal flexions and versions, chronic inflamma- 

1 Illustrations of various forms of malformation of the cervix may be found in 
the translation by McLaren of Courty's " Diseases of the Uterus, Ovaries," etc., 1883. 



438 THE ORGANS OF GENERATION. 

tions, repeated pregnancies, myomata, and accumulations of blood or 
mucus in the uterine cavity. Enlargement of the vaginal portion may 
be produced by the above causes, and is also found without known cause. 
One or both lips of the cervix may be uniformly increased in size, or 
they may be lobulated. 

Dilatation of the uterus is produced by accumulations of blood, 
mucus, or pus in consequence of narrowing or obliteration of the cervix 
or vagina. The uterine walls may retain their normal thickness, be 
thickened or thinned. The most frequent position of the stenosis is the 
os internum. The retained contents after a time change in character, 
forming a thin, serous fluid — liydrometra—OY they may be mixed with 
blood. The dilated uterus is not usually larger than an apple, but it 
sometimes reaches enormous dimensions. If both os internum and os 
externum are closed, the cervical cavity may be also dilated and the 
uterus have an hour-glass shape. If the obstruction is in the vagina, 
the uterus and vagina may form a large, flask-shaped body, and the line 
of demarcation between cervix and vagina be lost. In some cases the 
dilatation is confined to the cervix. If the obstruction is not complete, 
the retained fluid may escape into the vagina and afterward accumulate 
again. 

Accumulation of menstrual blood in the cavity of the uterus — hcema- 
tometra — is usually produced by congenital stenosis of the cervix or 
vagina. The dilated uterus may reach an enormous size. If the fluid 
is not evacuated by surgical interference, there may be either rupture or 
ulcerative perforation of the uterus. The blood may escape into the 
abdominal cavity, or be shut in by adhesions, or perforate into the blad- 
der or intestines. Sometimes the blood passes into the Fallopian tubes, 
dilates them, and escapes through their abdominal ends. 

CHANGES IN POSITION. 

The body of the uterus may become fixed in an abnormal position, 
while the situation of the cervix is unchanged. The body may be bent 
forward — anteflexio?i ; backward — retroflexion; or sideways — lateral 
flexion. The flexion may be slight, or so great that the neck and body 
form an acute angle. Anteflexion is the most common variety, and that 
in which the flexion is greatest. Peritoneal adhesions, flaccidity of the 
uterine walls, particularly after delivery, atrophy of the walls, ovarian 
and other tumors, etc., are the usual causes of flexions. 

The Versions of the uterus consist in an abnormal inclination of the 
long axis of the organ to that of the vagina. The uterus may be inclined 
backward, forward, or to one side. 

Retroversion is very much the most common. The fundus uteri is 
directed backward and downward; the cervix, forward and upward. This 
condition is found in various degrees; in the highest, the fundus lies in 



THE ORGANS OF GENERATION. 439 

Douglas'' cul-de-sac with the cervix upward, so that the axis of the uterus 
is parallel to that of the vagina, but in a direction nearly opposite to the 
normal one. Abnormal looseness of the uterine ligaments, abnormally 
large capacity of the pelvis, hypertrophy or tumors of the uterus, and 
pregnancy during the first four months, are some of the more common 
conditions under which this lesion occurs. 

Anteversion. — Inclination of the fundus forward and downward, and 
of the cervix backward and upward, is not common and seldom reaches 
a high degree. It occurs under the same general external conditions as 
anteflexion. 

Laferoversion is not very common as a simple lesion, but is not 
infrequently combined with other displacements. It may be produced 
by congenital shortening of one of the broad ligaments, by adhesions, or 
by the pressure of tumors. 

The greater degrees of version may produce very grave lesions. The 
urethra and rectum may be compressed. Cystitis, perforation of the 
bladder, dilatation of the ureters and hydronephrosis, and fatal obstruc- 
tion of the bowels may follow. If pregnancy exists, abortion may take 
place, or the inverted uterus may be forced through the peritoneum and 
posterior wall of the vagina and project through the vulva. In the non- 
pregnant uterus, pressure on the veins and consequent chronic inflam- 
mation of the organ may follow. 

Prolapsus Uteri Consists of a descent of the uterus into the vagina. 
The uterus may be only slightly lowered or it may project at the vulva. 
In complete prolapse we find a tumor projecting through the vulva, 
partly covered by the distended vagina, and presenting the opening of 
the os externum near its centre. The bladder and rectum may be drawn 
down with the vagina or may remain in place. The exposed cervix and 
vagina usually become inflamed and sometimes ulcerated, or the mucous 
membrane may become thickened. The lesion is frequently complicated 
by hypertrophy of the cervix. 

Gradual prolapse, which is most frequent, may be due to an increased 
weight of the uterus, as in pregnancy, inflammatory enlargement, the 
presence of tumors, etc. ; or to some abnormal condition of the uterine 
supports. It is frequently caused by a vaginal cystocele or rectocele. 
Sudden prolapse is most apt to occur in an enlarged uterus or one unduly 
heavy by reason of tumors connected with it. It is most common in sub- 
involution after parturition. 

Elevation of the uterus is produced by mechanical causes crowding or 
dragging it upward, as adhesions, tumors, etc. The vagina is drawn 
up and lengthened, and the vaginal portion of the cervix may be oblit- 
erated. 

Inversion of the uterus consists of an invagination of the fundus. 
The fundus may be invaginated in the body, the fundus and body in the 



440 THE ORGANS OF GENERATION. 

cervix, or the entire organ in the vagina. It usually occurs when the 
uterine walls are relaxed, and is very frequently due to traction on the 
placenta during parturition. It may take place spontaneously after par- 
turition. It may be produced by intra-uterine tumors. The mucous 
membrane of the inverted organ is frequently inflamed, particularly 
when the inversion is complete. 

Her nice of the uterus are rare. Ventral hernia may occur during 
the latter months of pregnancy, the peritoneum, aponeuroses, and skin 
being forced outward to form a sac in which the uterus lies. Crural 
hernial are produced by the drawing down of the uterus and ovaries into 
the sac of an intestinal hernia. Inguinal hernia may be produced in 
the same way or be congenital. Ischiatic hernia has been seen. Preg- 
nancy may occur in the uterus while situated in a crural or inguinal 
hernia. 

RUPTUEE AND PERFORATION. 

Rupture of the unimpregnated uterus is rare. It may, however, 
occur when the uterine cavity is distended with blood or serum, or in 
connection with large myomata of the uterine walls. 

In the gravid uterus, ruptures have been seen in nearly every month 
of pregnancy, but most frequently toward the end. The rupture may 
be produced by thinniug of the uterine wall by tumors, or by violent con- 
tusions, or as the result of cicatricial contraction of the os. 

The act of parturition is the most frequent cause. Malpositions of 
the foetus, narrowing of the pelvis, protracted labor, thinning of the 
uterine wall from tumors, forcible use of the forceps and other instru- 
ments, are the ordinary causes. The rupture may be in the body of the 
uterus or the cervix, or both; it may be large or small; it may extend 
completely or only partly through the uterine wall. The consequences 
of partial rupture are haemorrhage, gangrenous inflammation of the 
edges of the rupture, peritonitis, and usually death. In rare cases, the 
rupture cicatrizes and the patient recovers. Complete rupture usually 
causes death in a short time. The foetus escapes partly or completely 
into the abdominal cavity. If the patient survives the immediate shock, 
fatal peritonitis soon ensues. In rare cases, the foetus is shut in by ad- 
hesions and the patient survives. 

Perforations of the uterus may be produced by carcinoma, by abscesses 
in its neighborhood, and by ovarian cysts. 

HYPEREMIA — UTERINE AND PERI-UTERINE HEMORRHAGE. 

Hyperemia, — Aside from the active menstrual hyperemia, the uterus 
may be hypersemic in acute and chronic inflammation, as a result of dis- 
placement of the organ, and in certain forms of heart disease. The organ 
is usually enlarged, the mucous membrane swollen, and the veins more 
or less evidently dilated. 






THE ORGANS OF GENERATION. 441 

Hemorrhage. — Effusion of blood into the cavity of the uterus occurs 
normally at the menstrual periods. For the abnormalities to which this 
function is subject, we refer to works on gynecology. Effusions of blood 
at other than the menstrual periods may be caused by mechanical hyper- 
emia, by haemorrhoids, by acute hyperemia, by intra-uterine polypi and 
other tumors, by acute and chronic inflammation, by typhus fever, 
scurvy, etc., by ulcerating carcinoma, by abortions and miscarriages. 

A peculiar form of hemorrhage is the polypoid hematoma, or fibrin- 
ous polypus of the uterus. It occurs after parturition and after abor- 
tions. The portion of the uterine wall where the placenta was attached, 
with or without a portion of retained placenta, forms the point of attach- 
ment of the pedicle of the polypus. We find a large, polypoid, bloody 
mass firmly attached by a pedicle to the uterine wall. The uterus en- 
larges with the growth of the polypus; the cervix is dilated, and the 
thrombus projects into and may even fill up the vagina. The formation 
of such a thrombus is accompanied by repeated hemorrhages. 

Hemorrhage in the substance of the uterus occurs in old age. The 
mucous membrane and uterine wall are infiltrated with blood, and there 
is some blood in the uterine cavity. 

Peri-uterine or Retro-uterine Hcematocele consists in an accumulation 
of blood around the uterus or in Douglas' cul-de-sac. It may consist of 
blood extravasated into the abdominal cavity, which settles into the pel- 
vis; or, in consequence of local hyperemia, there may be repeated extra- 
vasations of blood. In the latter case, the local peritonitis may produce 
false membranes, between the layers of which hemorrhages take place. 
A similar condition rarely occurs in the male. The hemorrhagic mass 
may become incapsulated, or may soften or suppurate and perforate into 
the rectum or vagina, or may be absorbed. A form of extra-peritoneal 
hematocele is described in which the blood lies between the folds of the 
broad ligament. The extravasation may proceed from hemorrhage of 
any of the abdominal viscera or rupture of aneurisms; from vascular new- 
formed false membranes; from rupture of the varicose veins of the 
broad ligaments; from rupture of hemorrhagic cysts of the ovaries; 
from the Fallopian tubes in tubal pregnancy or in hematometra; or 
from general causes, such as scurvy, purpura, etc. In some cases the 
extravasation begins at a menstrual period, and increases at the succeed- 
ing periods. 

Ante-uterine Hcematocele is of occasional occurrence, either in con- 
nection with the retro-uterine form or when the posterior cul-de-sac is 
obliterated. 

35 



442 



THE ORGANS OF GENERATION. 



INFLAMMATION. 

/. Of the Unimpregnated Uterus, 

Acute Catarrhal Endometritis. — In this disease, which in its lighter 
grades may leave but little alteration after death, the mucous membrane 
is swollen, hypersemic, and sometimes the seat of punctate haemorrhages. 
The epithelium may desquamate, and the mucosa contain an undue 
quantity of small spheroidal cells. The surface is more or less thickly 






A 



^Si 



HH 



i 



:%PV& 




If 



'■V'".;-'< 






Fig. 185.— Chronic Endometritis with the Formation of a Polypoid Outgrowth from the 

Mucous Membrane. 

covered with muco-purulent exudation. In severe cases, shreds of mu- 
cous membrane may be exfoliated. The lesion is usually most marked 
in the mucous membrane of the body, but may involve the cervix at the 
same time, or the cervix alone. The body of the uterus may be swollen 
and hypergemic. Acute catarrhal inflammation may be due to injury, 
exposure during menstruation, the gonorrheal infection, or it may 
accompany acute infectious diseases. 



THE ORGANS OF GENERATION. 



443 



Chronic Endometritis. — This may be a continuation of an acute in- 
flammation or begin as a chronic disease. In some of the lesser degrees 
of inflammation we find but slight changes after death. The mucous 
membrane, on the other hand, may be swollen, hyperaemic, and covered 
with muco-purulent exudation. In other cases, there is more or less 
well-marked thickening of the mucous membrane, which may present a 
smooth or a rough, papillary surface or polypoid outgrowths (Fig. 185). 
Owing to the hypertrophy of the uterine glands in this condition, these 
papillary outgrowths, which are not infrequently scraped off by the sur- 
geon, often present the appearance of adenomata. Sometimes a thick 




te*2f 










W 

9 



-k 



^/uAietj. 



I 



■■:j 



'z~^a. 



Fig. 186. - Chronic Endometritis with the Formation of a Thick Layer of New-formed, very 
Vascular Tissue over the Surface of the Mucous Membrane. 

a, uterine muscle tissue; b, mucous membrane of uterus; c, new formed vascular tissue. 

layer of new-formed, very vascular tissue develops over the surface of 
the mucous membrane, largely covering in the uterine glands (Fig. 186). 
From the decomposition of extravasated blood in the mucous membrane, 
the latter may be mottled with brown or black. The glandular elements 
of the mucosa may be partially or almost entirely destroyed. The 
papillae of the cervix may be hypertrophied, the mucous follicles swollen 
and their outlets obstructed, leading to the formation of the so-called 
ovula Nabothi. The uterine wall becomes flaccid and atrophied, or it 
may be hypertrophied, especially in the cervical portion. Ulceration of 



444 THE ORGANS OF GENERATION. 

the mucous membrane, especially of the cervix, may occur. Contrac- 
tion or obliteration of the cervical canal may occur. The inflammation 
may extend to the Fallopian tubes or to the vagina. 

Chronic endometritis may exist at any age, but is most common 
after puberty, and is produced by a great variety of causes. It may 
occur in ill-nourished persons or in those suffering from exhausting 
diseases. It may be due to displacements and tumors of the uterus, sub- 
involution, injuries, etc. 

Croupous Endometritis. — This form of inflammation is not very com- 
mon. It occasionally occurs in the puerperal uterus, in acute infectious 
diseases, cholera, typhoid fever, the exanthemata, etc. The disease 
sometimes involves the vagina and Fallopian tubes. It may co-exist 
with croupous inflammation of the colon. 

Tubercular Endometritis. — This usually occurs as part of a tubercu- 
lar inflammation of the geuito-urinary tract. We find a part or the whole 
of the cavity of the uterus lined with a rough, yellowish or gray, cheesy 
mass, which may deeply involve the muscular walls of the organ. At 
the edges of the ulcerating cheesy areas we may find well-defined miliary 
tubercles, or we may find tubercles scattered through the otherwise in- 
tact mucosa. The lesions resemble those of tubercular nephritis. 

Syphilitic Endometritis. — The results of this infection are usually 
confined to the cervical portion, and consist of shallow or deep ulcera- 
tions and condylomata of the mucous membrane; or there may be a dif- 
fuse thickening of the mucosa. 

Acute Metritis is usually the result of acute catarrhal endometritis. 
The organ is swollen, succulent, congested; the mucous membrane cov- 
ered witli muco-pus; the peritoneal coat congested. There may be small 
extravasations of blood in the wall or cavity of the uterus. The inflam- 
mation, in rare cases, becomes suppurative, and abscesses are formed in 
the uterine wall. These may perforate into the peritoneal cavity or into 
the rectum. 

Chronic Metritis is the result of an acute metritis or accompanies 
acute or chronic endometritis, and is dependent upon the same condi- 
tions : subinvolution, displacements, tumors, active irritants, etc. The 
uterus is enlarged, the wall congested, thickened, and soft, or, owing to 
the new formation of connective tissue, hard and dense. The lesion may 
be most marked in the body or in the cervical portion. 

Perimetritis. — The peritoneal coat of the uterus may be inflamed, 
with the production of membranous adhesions or of pus. The adhesions 
may be small or very extensive, and, owing to their contractions, may 
cause various distortions and displacements of the pelvic organs. The 
inflammation is usually an accompaniment of chronic metritis and endo- 
metritis. In prostitutes, such adhesions are of very common occurrence. 

Parametritis, — The connective tissue about the uterus, between that 



THE ORGANS OF GENERATION. 445 

organ and the reflexions of the peritoneum, may be the seat of suppura- 
tive inflammation. It most frequently causes the death of the patient, 
but may result in the formation of dense connective tissue about the 
uterus. 

77. Of the Pregnant Uterus. 

The forms of inflammation which have just been described may 
attack the pregnant uterus. Catarrhal endometritis may produce effu- 
sion of serum, extravasations of blood, and abortions. Metritis may 
lead to softening of the uterine wall, so that ruptures take place during 
labor. Perimetritis and parametritis produce adhesions and abscesses 
about the uterus. 

Puerperal Inflammation. 

For a week or more after delivery, we fiud the inner surface of the 
still dilated uterus rough, especially at the insertion of the placenta, and 
covered with blackened, gangrenous-looking shreds of blood, mucous 
membrane, and placenta. This condition is not to be mistaken for in- 
flammation. 

As a result of some injury to the uterus during or after delivery, and 
the action of some infectious material which may gain access to the 
tissues, the puerperal uterus is liable to become the seat of a series of 
severe and often destructive inflammatory and necrotic changes. These 
may be confined to the uterus; they may induce serious alterations in 
surrounding parts; they may lead to an involvement of the peritoneum, 
or to pyaemia and its accompanying lesions in the most distant parts of 
the body. In one series of cases, a more or less extensive gaugrenous 
inflammation of the mucous membrane and the underlying parts may 
lead to the casting-off of larger and smaller shreds of necrotic tissue, and 
the formation of deep and spreading ulcers, which may be accompanied 
by severe parametritis and fatal peritonitis. This condition may be due 
to injury or to the presence of decomposing portions of retained pla- 
centa. In other cases the inflammation has a croupous character, which 
may affect the vagina and lead to necrosis and gangrene, ulceration, and 
peritonitis. In connection with either of the above forms of inflamma- 
tion, or without them, there may be thrombosis of the uterine sinuses, 
purulent inflammation of the veins, suppuration and abscess in the ute- 
rine wall, and, owing to the generalization of the infectious material, to 
metastatic abscesses in the lungs, spleen, kidneys, etc. Or acute pleu- 
risy, ulcerative endocarditis, purulent inflammation of the joints, hyper- 
plastic swelling of the spleen and lymph nodes, may furnish character- 
istic features of the presence of an acute infectious disease. In some 
cases which rapidly pass to a fatal termination, the local lesions may be 
but slightly marked, and general alterations characteristic of pysemia, 
such as metastatic abscesses, etc., be entirely wanting. 



446 THE ORGANS OF GENERATION. 

Bacteria, in the form of micrococci, are very constantly present in 
the exudation, in the lymph vessels, veins, and inflamed tissue of the 
uterus (see Fig. 187); often in enormous quantities in the peritoneal 
exudation and in the metastatic inflammatory foci. There is good 
reason for believing that the destructive local processes are due to the 
presence and action of micrococci, and that the general infection in this, 
as in other forms of septicaemia and pyaemia, is dependent upon the 
same cause (see Septicaemia). 

The Streptococcus pyogenes has been found in a considerable num- 
ber of cases, and is believed to induce the puerperal inflammation. 

•v"- ■• ■>' ■'-'■-■ _-- ' ~/f\-\- .'■*'' ' i— -^- --_/v ;;; 'U- ■.■>/./ ■■■• '■*..'• X, 



Fig. 187. — Uterine Phlebitis following Delivery with Retained Placenta. 
Death 9 days after delivery. Micrococci in the walls of the inflamed veins stained with fuchsin. 

ULCERATION AND DEGENERATION. 

Catarrhal, tubercular, and syphilitic ulceration have been mentioned 
above. 

Phagedenic or Corroding Ulcer. — This rare form of ulceration usu- 
ally occurs in old age, without assignable cause. It begins in the cervix 
and gradually extends until it may destroy the greater part of the uterus 
or even invade the bladder and rectum. The ulcer is of irregular form; 
its base is rough and blackish, its walls indurated. It should not be 
confounded with carcinomatous ulcer, which it considerably resembles. 

Fatty Degeneration. — This may occur in connection with inflamma- 
tory changes, in acute infectious diseases, and in phosphorus poison- 
ing. 



THE ORGANS OF GENERATION. 



Amyloid Degeneration in the uterus is of rare occurrence, 
affect the muscle fibres or the walls of the blood-vessels. 



44? 

It may 



TUMORS. 

Fibromata. — Dense nodular fibromata of the uterus are exceedingly 
rare, the so-called fibromata being in most cases myomata or fibro-myo- 
mata. Fibroma papillare, on the other hand, is a common form of 
growth from the mucous membrane. It consists of a more or less vas- 
cular connective-tissue stroma covered with epithelium. The surface 
may be smooth or villous. It may contain very numerous gland folli- 
cles, and then approaches the type of adenoma, or even carcinoma. 
The stroma may be loose and succulent, and resemble mucous tissue, 




Fig. 188. — Adenomatous Hyperplasia of the Uterine Mucous Membrane. 
This section is from a large polypoid outgrowth which protruded from the cervix uteri. 

forming the so-called mucous polypi; and these again may contain 
glandular structures. In any of these forms the blood-vessels may be 
abundant and dilated, forming telangiectatic or cavernous polypi. The 
adenomatous polypi may become cystic from the dilatation of the gland 
follicles. 

Polypi of the uterus may be multiple or single, small or large. 
Numerous smaller and larger papillary outgrowths from the mucous 
membrane may occur in chronic endometritis. Single polypi may grow 
from the mucosa of the body of the uterus or from the cervix, and hang- 
by a long pedicle down into the vagina. 



4i8 THE ORGANS OF GENERATION. 

The large number of glandular structures in many of these chronic 
inflammatory, papillary, and polypoid outgrowths (Fig. 188) often 
justify the name of adenomatous hyperplasia of the mucous membrane 
or of adenomatous papillomata or polyps. 

Syphilitic papillary growths in the form of pointed condylomata may 
form finely papillary, wart-like excrescences of variable size, particularly 
on the cervix. 

Myomata. — These tumors, whose characteristic structural elements 
are smooth muscle cells (see Fig. 62), are the most common of uterine 
tumors and are frequently of no special practical importance, but are 
sometimes of very serious import. They are especially common in ne- 
groes. They are most frequently composed of both muscular and fibrous 
tissue — fibro-myomata — but the relative amount of the two kinds of 
tissue is subject to great variation. They are most apt to occur after 
puberty, and usually in advanced life. They may be single or multiple, 
small or of enormous size; are usually sharply circumscribed, whitish or 
pink, dense and hard, or sometimes soft, and present on section inter- 
lacing bands or irregular masses of glistening tissue. Their favorite 
situation is in connection with the body of the uterus, but they may 
occur in the cervix or in the folds of the broad ligaments. According 
to their position, we may distinguish subserous, submucous, and intra- 
parietal forms. The subserous myomata grow from the outer muscular 
layers of the uterus in the form of little nodules. As they increase in 
size they may become separated from the uterine wall and remain attached 
only by a narrow pedicle or by a little connective tissue. They may w 7 ork 
their way between the folds of the broad ligament until they are at some 
distance from their point of origin. Some authors mention cases in 
which the tumors became entirely detached from the uterus and w r ere 
free in the abdominal cavity. In some cases, the tumors excite inflam- 
mation of the adjacent peritoneum, leading to the formation of adhesions 
or of collections of pus. Cases are recorded in which, owing to the 
atrophy of the pedicle, subserous myomata have become completely de- 
tached from the uterus and were held in place and nourished by perito- 
neal adhesions. In other cases, the tumor reaches a large size, but 
remains firmly attached to the uterus. This organ may then be drawn 
upward, the cervix and vagina being elongated and narrowed. The 
traction may be so great that the body of the uterus 'is entirely separated 
from the cervix. The bladder may also be drawn upward, producing 
incontinence of urine and cystitis. Subserous myomata are very often 
multiple and frequently attain great size. 

The Submucous Myomata grow from the inner muscular layers of the 
uterine wall. They commence as rounded nodules which lift up the 
mucous membrane. Their usual position is the fundus uteri. They 
rarely occur in the cervix. As the tumors increase in size they project 






THE ORGANS OF GENERATION. 449 

into the uterine cavity. They then remain continuous with the uterine 
wall over a large area, or are attached by a large or small pedicle. They 
are usually well supplied with vessels. The uterus dilates with the 
growth of the tumor, and its walls may be also thickened. The tumor 
may reach such a size as to entirely fill the cavity of the dilated uterus 
and project through the cervix into the vagina. 

The submucous myomata are usually single, although there may be 
at the same time subserous and intraparietal tumors. They are fre- 
quently soft. If they are of large size and polypoid in form, they may 
project through the cervix and drag down the fundus of the uterus, 
producing inversion. The mucous membrane covering them may be 
atrophied or hyperaemic, with dilated blood-vessels, and may thus give 
rise to severe and repeated haemorrhages. Haemorrhage may occur in 
the substance of these tumors. Inflammation, suppuration, and gan- 
grene may also occur. The surface may be ulcerated. In some cases 
the pedicle of the tumor is destroyed, and it is spontaneously expelled. 

The intraparietal myomata grow in the substance of the uterine 
wall, but, if they attain a large size, project beneath the serous or the 
mucous coat. They are found in every part of the uterus, but are most 
frequent in the posterior wall. 

The shape of the uterus is altered in a great variety of ways by the 
presence of these tumors; its cavity is narrowed, dilated, or misshapen; 
it undergoes flexion and version in every direction. The tumors may 
sink downward and become attached to the posterior wall of the 
vagina, looking as if they grew from it. They may, without the forma- 
tion of a pedicle, project into the cavity of the uterus, fill it up, and 
project through the cervix. The uterus is dilated, its wall hypertro- 
phied or atrophied. 

The tumors themselves may undergo a variety of secondary altera- 
tions. The muscle fibres may undergo fatty degeneration, and the 
tumor diminish in size, or even undergo, it is said, entire destruction 
and atrophy. Calcification may occur, converting a part or the whole 
of the tumor into a stony mass. The intraparietal and submucous myo- 
mata may give rise to profuse haemorrhages; they may suppurate and 
become gangrenous. 

Sometimes the tumors or circumscribed portions of them are very 
vascular, constituting the telangiectatic or cavernous variety. These 
tumors, which possess some of the characters of erectile tissue, may sud- 
denly change in size from a variation in the amount of blood which they 
contain. 

A very important change which is sometimes found in these tumors 

is the development of cysts in their interior (fibro-cystic tumors). This 

sometimes takes place in those tumors which grow outward beneath the 

peritoneal coat. We find one or more cavities communicating with each 

36 



450 THE OKGANS OF GENERATION. 

other, with rough, trabeculated walls. The appearance is more that of 
cavities than of cysts. There may be a number of smaller cavities, or 
they may fuse to form one large one. The 'fluid contained in the cavi- 
ties is like synovia, or is mixed with blood. These cystic myomata 
may reach an immense size and fill the abdominal cavity. The diag- 
nosis, during life, between them and ovarian cysts is often very difficult, 
and they have frequently been the subjects of fatal operations. 

In the cervix uteri, myomata are rare. They may grow as polypi 
beneath the mucous coat, or produce enlargement of the anterior or pos- 
terior lips, or may grow outward into the abdominal cavity. 

Combinations of myoma and sarcoma sometimes occur — myosar- 
coma. 

Sarcomata may occur as primary tumors in the mucous membrane of 
the uterus, either in the form of a diffuse infiltration or as a circum- 
scribed nodular or polypoid mass. They frequently involve the muscu- 
lar wall, are liable to haemorrhage and gangrene, and, particularly in 
the diffuse form, are liable to recur after removal. They may consist 
largely of spindle or spheroidal cells, or both. It is said that sarcoma of 
the uterus is more liable to occur at an advanced age than at an early 
period, as is the rule with sarcomata of other organs. 

Angioma. — A small, cavernous angioma of the wall of the uterus has 
been described. 

Carcinoma. — The carcinomata of the uterus commence most fre- 
quently in the cervix and portio vaginalis, and the most common form 
is the epithelioma. The growth of epitheliomata of the cervix uteri 
proceeds under three tolerably distinct forms, which, however, fre- 
quently merge into one another. 

1. The Flat, Ulcer ating Epithelioma. — This form of cancer commences 
as a somewhat elevated, flat induration of the superficial layers of the 
cervix, sometimes circumscribed, sometimes diffuse. This induration 
is due to the growth of plugs and irregular masses of epithelial cells 
into the underlying tissue. Ulceration usually commences early, and 
may proceed slowly or rapidly. The edges of the ulcer are irregular, 
indurated, and somewhat elevated. The ulceration of the new-formed 
cancerous tissue at the edges is usually progressive, so that the vaginal 
portion of the cervix, the cervical canal, the vagina, and even the blad- 
der and rectum may be involved. More or less extensive haemorrhages 
and necrosis of the base of the ulcer are liable to occur. The entire 
cervix may be destroyed. 

2. In another class of cases, the carcinomatous growth develops 
under the form of papillary or fungous excrescences, which may form 
larger or smaller masses composed of epitheliomatous tissue. Hand-in- 
hand with this projecting growth there may occur an epithelial infiltra- 
tion of the underlying tissue of the cervix. These growths are often 



THE ORGANS OF GENERATION. 



451 



quite vascular, and may give rise to severe haemorrhages. They may 
ulcerate, and thus produce great destruction of tissue. 

3. In still another class of cases, there is a more or less deep infiltra- 
tion of the submucous tissue, either diffuse or in circumscribed nodules, 
with epithelial cell masses. We find at first, in the vaginal portion of 
the cervix, in the submucous connective tissue, either nodules or a 
general infiltration of a whitish new growth. The cervix then appears 
large and hard. Very soon the mucous membrane over the new growth 
degenerates and falls off; the superficial layers of the new growth under- 




■A 



iV) k III 



■ A 



/i 









Fig. 189.— Carcinoma of the Cervix Uteri (Ulcerating). 

go the same changes. After this, the formation of the new growth and 
its ulceration go on simultaneously, producing first an infiltration and 
then destruction of the cervix, and often of a part of the body of the 
uterus. The growth frequently extends to the vagina, the bladder, and 
rectum with the same destructive character, so that we often find the 
cervix and upper part of the vagina destroyed, and in their place a large 
cavity with ragged, gangrenous, cancerous walls (Fig. 189). Less fre- 
quently the pelvic bones are invaded in the same way. Not infrequently 
the ureters are surrounded and compressed by the new growth, so that 
they become dilated. The dilatation may extend to the pelves and calyces 



-±52 THE ORGANS OF GENERATION. 

of the kidneys. The new growth may begin in the cervix, and extend 
uniformly over the internal surface of the cervix and of the body of 
the uterus. The entire uterus is converted into a large sac, of which 
the walls are infiltrated with the new growth, while the internal surface 
is ulcerating and gangrenous. Jn some cases there is a considerable 
formation of new, dense connective tissue, so that the growth has a scir- 
rhous form. 

In rare cases, the growth begins in the upper part of the cervix or in 
the body of the uterus, while the lower part of the cervix is not involved. 
In all of these cases, the epithelial cells of the new growth follow more 
or less closely the type of the epithelial cells of the part from which they 
spring. 

In still another class of cases, in which the new growth may be in the 
form of nodules, or diffuse infiltrations, or polypoid masses, or may pre- 
sent more or less extensive alterations, the cells are irregular, polyhedral 
in shape, the tumor belonging to the class of glandular or medullary 
carcinomata. These also usually commence in the cervix and, according 
to the views of many writers, probably in the mucous glands. 

In rare cases the entire wall of the uterus is infiltrated with the new 
growth, and the organ is much enlarged. Colloid carcinoma sometimes 
occurs, but is rare. 

While we may for convenience recognize the above types of carcinoma 
of the uterus, it should be borne in mind, as above stated, that they are 
not apt to be perfectly distinct, and some of them may merge into one 
another or exist simultaneously. Exudative inflammation is of frequent 
occurrence in these as in other tumors of the uterus (see Fig. 72). 

As a result of the ulceration of these various forms of carcinoma, 
recto-vaginal fistulae may be formed; the lumbar lymph nodes may be 
involved, and metastases in distant organs are occasionally though not 
frequently formed. Frequent and profuse haemorrhages, gangrenous 
destruction of tissue, the absorption of deleterious materials, etc., are 
apt to lead- to the development of a more or less profound anaemia and 
cachexia. 

PARASITES AND CYSTS. 

Various forms of "bacteria are of frequent occurrence. Echinococcus 
has been found in the body and neck of the uterus, and may rupture into 
the peritoneal cavity or into the vagina. 

Cysts. — Aside from the cysts which develop in tumors of the uterus, 
in the cervix uteri the mucous follicles are frequently so dilated as to 
form cysts filled with a gelatinous material and more or less epithelium. 
These cysts may be large or small, and are frequently called ovula Nabo- 
thi. Sometimes there is an inflammatory growth of new connective tis- 
sue about these cysts. In other cases the cysts may project from the 



THE ORGANS OF GENERATION. 453 

mucous membrane in the form of polypi. Similar changes are infre- 
quently found in the body of the uterus from the dilatation of occluded 
uterine glands. Dermoid cysts are rarely found in the walls of the 
uterus. 

THE OVARIES. 

MALFORMATIONS. 

One or both ovaries may be absent, the other organs of generation 
being also absent or undeveloped. Or the ovaries may be only partially 
developed. Absence or arrest of development of one ovary is sometimes 
met with in otherwise well-formed individuals. It is sometimes accom- 
panied by a low position of the kidney on the same side. The ovaries 
may pass into the inguinal canal or into the labia majora, and remain 
fixed there through life. Less frequently they are found in the crural 
canal or the foramen ovale. 

CHANGES IN SIZE. 

The ovaries may become larger than normal by chronic inflammation, 
by the formation of cysts and tumors. They may become atrophied in 
old age, the Graafian follicles disappearing, and the organ shrivelling into 
a small, irregular, fibrous body. Atrophy may be produced by ascites, by 
chronic inflammation, or from unknown causes. As the result of the 
maturing and rupture of the Graafian follicles, with and without preg- 
nancy, the surface of the ovary, which before puberty is smooth, maybe- 
come roughened by irregular cicatricial depressions. 

CHANGES IN POSITION. 

In adult life, the ovaries may pass as hernias into the inguinal or cru- 
ral canal, the foramen ovale, or the umbilicus. 

The position of the ovaries in the abdomen may be changed by the 
pressure of tumors, the traction of false membranes, etc. It may occur 
in enlarged ovaries or in those of normal size, and by the compression of 
the veins may lead to congestion and chronic inflammation of the organ. 

HYPEREMIA AND HEMORRHAGE. 

Aside from the normal hyperemia of the ovaries during menstruation, 
the vessels may be congested in inflammation, in displacements with in- 
terference with the venous circulation, in certain diseases of the heart, 
etc., and may then be followed by chronic inflammation. 

The menstrual periods are accompanied by the effusion of blood into 
a Graafian follicle. Normally the amount of blood is small, becomes 
solid, is decolorized, and then gradually absorbed. Sometimes the effu- 
sion of blood is much greater; the follicle filled with blood is as large as 
a pigeon's egg. The blood may remain in the follicle and be absorbed, 



454 



THE ORGANS OF GENERATION. 



and replaced by a serous fluid, or it may rupture it and escape into the 
peritoneal cavity. Death may ensue from the hemorrhage, or the blood 
may collect in Douglas' cul-de-sac and be inclosed in false membranes. 
Haemorrhages also occur in follicles which have become cystic. Inter- 
stitial haemorrhage in the ovary sometimes occurs without known cause. 

INFLAMMATION (OOPHORITIS). 

Acute Inflammation of the ovaries occurs most frequently in the puer- 
peral condition, either as part of a general peritonitis or as a primary 
affection. 

With puerperal peritonitis, both ovaries are usually inflamed ; they 
are swollen, congested, soft, infiltrated with serum or pus, or gangren- 
ous. The inflammation may attack principally the capsule, the stroma, 




Fig. 190.— Chronic Oophoritis with dilated Blood-vessels and Cysts. 
a, dense connective-tissue stroma; &, dilated veins; c, cysts; d, cyst with granular contents; 
cortical zone of immature Graafian follicles. 



or the follicles. Inflammation of the capsule results in adhesions and 
collections of pus, shut in by false membranes; of the stroma, in ab- 
cesses and fibrous induration; of the follicles, in their dilatation with 
purulent serum. If the inflammation of the ovary is the primary lesion, 
it is usually confined to one organ. The stroma of the ovary is infiltrated 
with serum and pus, and may contain abscesses of large size. In other 
cases the ovary itself is but little changed, but is surrounded by a mass 
of fibrinous and purulent exudation. Such idiopathic forms of inflam- 
mation may terminate in recovery; or the abscesses may perforate into 
the rectum and vagina; or the ovary is left indurated and bound down 
by adhesions; or the patient dies from the violence of the disease. 



THE ORGANS OF GENERATION. 455 

Inflammation of the ovaries unconnected with the puerperal condi- 
tion is not common, but it may occur in connection with acute or 
chronic peritonitis or perimetritis. It is usually confined to one ovary. 
Either the follicles, stroma, or capsule, or all together, may be involved. 
The inflamed follicles are enlarged, their walls thickened; they may 
contain bloody or purulent fluid. The stroma becomes infiltrated with 
serum or pus, and later we may find abscesses or fibrous induration of 
the organ. The inflammation of the capsule may lead to the formation 
of membranous adhesions between the ovary, Fallopian tube, and sur- 
rounding parts. 

Chronic Interstitial Oophoritis is not infrequently preceded by an 
acute inflammation, or it may gradually develop as an independent con- 
dition, often determined by some mechanical interference with the blood- 

* L 




F 



w 



fU 






Fig. 191.— Chronic Oophoritis with Atrophy. 
From a case of valvular disease of the heart with chronic metritis and endometritis, a, thick- 
ened and dense interstitial tissue; b, old corpora lutea; c, arteries with greatly thickened walls: 
d, dilated vehos. 

current. The organ may be increased in size, owing to the formation of 
loose cellular, or of dense, firm, new connective tissue. Under these con- 
ditions, the blood-vessels, especially the veins, may be widely dilated 
and cysts in varying number and size may be present (Fig. 190). Some- 
times the new-formed dense connective tissue may be largely limited to 
the surface of the organ, so that the albuginea may become so dense and 
thick that the functions of the organ must, as it would seem, be perma- 
nently interfered with. Under these conditions the surface of the ovary 
may be smooth or rough. 

On the other hand, the organ may be smaller than normal as the re- 
sult of the formation of dense new interstitial connective tissue, and its 
surface greatly roughened and distorted. Sometimes the formation of 



4:56 THE ORGANS OF GENERATION. 

new dense tissue may be largely confined to the walls of the arteries, 
which become prominent and tortuous. The atrophied ovary may be 
largely made up of thick- walled arteries and fibrous masses which are 
the result of incomplete resolution of the corpora lutea (Fig. 191). 

Tubercular Inflammation of the ovaries is rare, and may accompany 
tubercular inflammation of other organs, particularly the peritoneum 
and Fallopian tubes. Tt usually results in the production of cheesy 
nodules of considerable size. 

Syphilitic Inflammation iu the form of gummata is uncommon. 

TUMORS. 

Fibromata. — These tumors are not very common nor usually of great 
importance. They may be very small or of great size. They are usually 
dense in texture, and in a considerable number of cases seem to originate 
in the tissue formed in the closure of the ruptured Graafian follicle. 
They may contain cysts or be accompanied by cysts of the surrounding 
stroma. Papillary fibromata of the surface of the ovary are sometimes 
seen. 

Leiomyomata containing more or less fibrous tissue are of occasional 
occurrence. 

Sarcoma of the ovaries is not common. It is usually primary, but 
may be metastatic. It is usually of the spindle-celled variety, but may 
contain areas of spheroidal-celled tissue or more or less fibrous tissue. 
The tumors may be hard or soft, and are apt to involve both ovaries. 

Chondroma of the ovaries is described, but is rare; cartilage not in- 
frequently occurs, however, in dermoid cysts. 

Carcinoma, usually of the glandular variety, may occur as a primary 
tumor of the ovary. It may be due to a continuous infection from 
neighboring organs, or more rarely it is of metastatic origin. Although 
the glandular medullary carcinomata are the most common, scirrhous, 
melanotic, and colloid cancer sometimes occur. Some forms of carci- 
noma stand in very close relation with certain of the cystic adenomata 
(see below). 

Adenomata (Cystic Adenomata; Compound Ovarian Cysts). — These 
growths, which may occur in one or both ovaries, form one of the most 
common and important classes of ovarian tumors. Some of their most 
noteworthy and important features depend upon their tendency to the 
formation of cysts. It should be remembered, however, that the pri- 
mary lesion is a true new formation of glandular tissue, and not, as in 
the case of most cysts, a transformation, by retention or otherwise, of 
pre-existing structures. 

The growth primarily consists of a fibrous stroma, in which are 
tubular follicles lined with cylindrical epithelium. Or, in some cases, it 
consists of the above follicular or glandular structures associated with 



THE ORGANS OF GEx\ERATION. 



457 



papillary outgrowths from a fibrous stroma, which are covered with 
cylindrical, epithelium. Sometimes oue, sometimes the other form of 
growth — the glandular or the papillary — predominates (Fig. 192). 
There is, as above stated, a marked tendency, particularly in the glan- 
dular form of adenoma, to a dilatation of the follicles by a semi-fluid 
material, and the formation of cysts. There may be a number of follicles 
equally dilated, so as to form a number of cysts of moderate size; or only 
a few follicles are enormously dilated to form a large multilocular cyst 
with but few compartments. The walls of the cysts may fuse together, 
and be absorbed so as to form one large cyst divided by incomplete septa 
— unilocular cysts. The stroma in which the follicles and cysts are im- 
bedded may be largely developed or very scanty. 




Fig. 192.— Cystic Adenoma of Ovary (Papillary form). 

The walls of the larger cysts are composed of fibrous tissue which is 
dense in the outer layers, more cellular in the inner, upon which the 
epithelium is placed. They ma}' .be thin and membranous, or we find 
developed on their internal surfaces an intracystic growth composed of 
a fibrous stroma and tubular follicles. These secondary follicles may 
also be filled with fluid and form larger and smaller cysts. The intra- 
cystic growths may be so large as to fill up the original cysts. Sometimes 
the intracystic growth presents very little dilatation of its follicles, so 
that the entire tumor has more the character of a solid growth than of a cyst. 

In many of the cysts in which the formation of follicles and their 
dilatation are well shown, the growth of the papillomatous projections is 
also seen, so that the cyst cavity may be more or less filled with cauli- 
flower-like tufts. 
37 



458 THE ORGANS OF GENERATION. 

The cylindrical epithelium lining the cysts usually forms a single 
layer, but, owing to the accumulation of fluid, the cells may become flat- 
tened and atrophied, or they may be fatty or desquamated. The con- 
tents of the cysts differ considerably in different cases, and even in dif- 
ferent cysts in the same case. It may be tough and ropy, or gelatinous 
or serous; transparent and colorless, or yellow or reddish, or reddish 
brown; or it may be turbid and colorless, or variously colored, red, 
brown, or chocolate. 

Chemically the cyst contents, when thick and ropy, contain mucin or 
paralbumen, and perhaps other less well-known compounds belonging to 
the same class. It is believed that the peculiar ropy character which 
the fluid often possesses is due to the paralbumen, but the chemical na- 
ture and relations of this substance are still matters of dispute. It is 
probable that the contents of these cysts are, so far as the mucin and 
paralbumen are concerned, produced by a metamorphosis of the proto- 
plasm of the lining ceils, similar to that by which the mucin is produced 
in the mucous glands and in mucous membranes. We frequently find 
tjie cylindrical cells presenting the form of the so-called "beaker cells," 




Fig. 193.— Cells from Contents op an Ovarian Cyst in a Condition of Fatty Degeneration. 

and in some cases the mucous contents of the cysts are seen to be con- 
tinuous with the similar contents of the beaker cells. It is probable 
that much of the fluid contents of the cysts comes from simple transuda- 
tion. 

Microscopically the contents of these cysts present also considerable 
variation. We may find almost no structural elements; or there may be 
red blood-cells in variable quantity, and pus cells in various stages of 
granular or fatty degeneration or of disintegration, so that variously 
shaped fragments of the cells appear. Then we may find cylindrical, or 
flattened, or polyhedral cells, either well preserved, swollen, or in a state 
of fatty degeneration (Fig. 193), or we may find fragments of these cells. 
It is these various forms of cells, often more or less swollen and in a con- 
dition of more or less well-marked granular and fatty degeneration, which 
have been considered characteristic of the ovarian cysts and are some- 
times called DrysdaWs corpuscles. While, however, they are of fre- 
quent occurrence under these conditions, they are by no means pathog- 
nomonic, since we find them in the contents of various kinds of cysts 



THE ORGANS OF GENERATION. 459 

and cavities where the cells are undergoing degeneration. In addition 
to the above structural elements, we may find free fat-droplets, chole- 
stearin crystals, pigment granules, and more or less granular detritus. 
The material filling these cysts is sometimes called colloid, and the cysts 
are frequently called colloid cysts; but we believe that the above view of 
their nature is the correct one. 

Numerous secondary changes are liable to occur in these cysts. The 
cells may become fatty and peel off, so that we may find in some parts 
only a connective-tissue wall. The walls may atrophy, may become in- 
filtrated with salts of lime, or contain concentrically lamellated lime con- 
cretions. Inflammatory changes may occur in them. There may be 
a suppurative inflammation of the walls leading to the formation of 
abscesses, or pus may be mingled with the cyst contents; the epithelium 
may be exfoliated and granulation tissue may form in the walls. 
Chronic inflammation may lead to considerable thickening of the walls, 
and to adhesions with neighboring parts. Haemorrhages, sometimes very 
extensive, may occur in inflammation, or as the result of other disturb- 
ances of the circulation, so that some of the cysts may be filled with 
blood. Inflammatory softening, gangrene, etc., of the walls may lead 
to perforation, so that the contents of the cysts may be discharged into 
the peritoneal cavity, or, in virtue of adhesions, into the bladder, vagina, 
or rectum. Perforation may be caused by the piercing of the walls by 
the papillomatous growth. Carcinoma may be developed from the epi- 
thelium of the cysts. Since these cysts sometimes reach a very large 
size, they may produce the greatest variety of disturbances in the ab. 
dominal cavity, which need not be enumerated here. 

They probably originate in the glandular epithelium of the ovary 
either before or after the formation of the Graafian follicles. 1 

Follicular Cysts of the Ovary. — The Graafian follicles may be dilated 
so as to form cysts. This may occur in one or both ovaries, and the 
cysts may be small or large, single or multiple. They are usually found 
after middle life, but may occur during youth, childhood, or even in 
the foetus. The follicles dilate from the accumulation of fluid within 
them; the ovum is destroyed, the epithelium flattened. The contents 
are usually serous and colorless, but may be viscid, turbid, purulent, or 
variously colored, red, yellow, or brown. The ovary may be crowded 
with numerous cysts of moderate size, whose adjacent walls may coalesce 
and atrophy, forming communications between them. 

A variety of this form of cyst is formed by the dilatation of a follicle 



1 For more extended descriptions of the cyst adenomata of the ovaries, see Wal- 
deyer, "Die epithelialen Eierstocksgeschwulste," Archiv fur Gynakologie, Bd. 1, 
Heft 2, pp. 252-316, 1870. Also Klebs, " Handbuch der pathologischen Anatomie," 
vierte Lieferung, p. 796, 1873. 



460 THE ORGANS OF GENERATION. 

containing a corpus luteum. Such cysts may communicate with a Fal- 
lopian tube. 

Dermoid Cysts. — These cysts may be uni- or multilocular, are usually 
of moderate size, but sometimes become as large as a man's head or 
larger. Their fibrous walls may be thick or thin, and portions of the 
internal surface may present more or less completely developed cuticular 
structures, such as corium, papillae, epidermis, hairs and hair follicles, 
sebaceous glands, etc. The cavity may contain a thick, whitish, greasy 
material composed of flattened epithelium, fat, or cholestearin crystals. 
Or the cavity or walls may contain masses of irregularly formed hair, 
teeth, bone, cartilage, striated muscle, and nerve fibres and cells. Such 
growths, which are doubtless of embryonal origin, may exist for many 
years without causing inconvenience; but inflammatory changes may 
occur in them, leading to adhesions and perforations into adjacent organs. 
They may form the nidus for the development of carcinoma, or they 
may calcify. 

In addition to the above-described adenoid, dermoid, and simple 
follicular cysts, there are a number of composite forms of not infrequent 
occurrence. Thus, in connection with dermoid cysts or separately, we 
find larger and smaller cysts lined with ciliated epithelium. Then there 
are several cases described of cysts which partake of the characters of 
both adenoid and dermoid cysts. Such cysts may be multilocular and 
be lined with flattened, cylindrical, or ciliated epithelium, and may con- 
tain epidermal cells, cholestearin or mucin, etc. 1 

Small cysts, sometimes pediculated, sometimes not, of doubtful 
origin and usually of no special significance, are frequently found grow, 
ing from the broad ligament near the ovary. The walls are usually very 
thin, lined with flattened epithelial cells, and the contents serous. 

Cysts of the Parovarium, lying between the peritoneal layers of the 
broad ligament, are usually small, but may be as large as a man's head. 
They are usually lined with ciliated epithelium, but sometimes with flat- 
tened non-ciliated cells. The contents may be serous or may be thick, 
and contain mucin and paralbumen, 

THE FALLOPIAN TUBES. 
MALFORMATIONS. 

Absence of both tubes occurs with absence of the uterus. One tube 
may be absent, with arrested development of the corresponding side of 
the uterus. Both tubes may be imperfectly developed; either of their 

1 A tolerably full bibliography of the tumors of the ovaries may be found in 
Tait's "Pathology and Treatment of Diseases of the Ovaries," 4th ed., Wm. Wood & 
Co., p. 131. 






THE ORGANS OF GENERATION. 461 

ends may be closed; they may be inserted into the uterus at an abnormal 
place; they may terminate in two or three abdominal ostia. 

CHANGES IN POSITION AND SIZE. 

The Fallopian tubes may participate in the various malpositions of 
the uterus and ovaries; but they are most frequently displaced by the 
contraction of adhesions formed in perimetritic and periovarial inflam- 
mations. 

The lumen of the tube may be partially or completely closed as the 
result of inflammation of the mucous membrane; of peritonitis about 
the fimbriated extremity; of tumors or inflammation of the uterus; or 
by pressure from without, as by adhesions, tumors, etc. It may become 
stopped by plugs of mucus or pus. 

Dilatation of the tubes may be produced by an accumulation of 
catarrhal or other exudation, when there is partial or complete stenosis 
at some portion of the tube. The dilatation may be moderate, convert- 
ing the tube into a tortuous, sacculated canal containing mucous or 
serous fluid; or, more rarely, large cysts may form containing several 
pounds of serous fluid — hydrosalpinx. As the fluid collects, the epi- 
thelium may become flattened or fatty or may desquamate. As a 
result of an inflammation in the walls of the dilated tube, the contents 
may be mixed with pus or blood. Eupture of a dilated tube sometimes 
occurs; or severe and even fatal haemorrhage may take place into its 
cavity. Papillary growths are sometimes found springing from the 
inner wall of the cysts. 

HAEMORRHAGE. 

Haemorrhage into the tube may occur in puerperal women with 
retroversion of the uterus, with abortions; haematometra and tubal 
pregnancy; in acute infectious diseases. The blood may undergo de- 
generative changes and be largely absorbed, or it may escape into the 
peritoneal cavity and cause peritonitis. 

INFLAMMATION (SALPINGITIS). 

Catarrhal Inflammation of the mucous membrane of the Fallopian 
tubes commonly occurs in connection with endometritis, frequently in 
the puerperal condition. In the acute stage, the mucous membrane is 
hyperaemic and swollen, and covered with a muco-purulent exudation. 
The inflammation may subside, leaving no lesions, but it more fre- 
quently becomes chronic, and may then result in peritoneal adhesions, 
obliteration of the tubes, and dilatation. 

Suppurative Salpingitis. — This inflammation of the mucous mem- 
brane may assume a suppurative character, particularly in connection 



462 THE ORGANS OF GENERATION. 

with puerperal metritis and peritonitis, but sometimes as a result of 
gonorrhoeal inflammation. 

Under these conditions, the wall of the tube may be involved, and 
pus may exude from the abdominal ends. It is difficult, in many cases 
of suppurative salpingitis associated with peritonitis, to say which is 
the primary lesion. 

In some cases, there is a considerable collection of pus in the tubes, 
causing dilatation — pyo-sa!pi?ix. These collections may rupture into 
the peritoneal cavity, or the pus may escape into a cavity shut in by 
adhesions, or may perforate into the intestine or bladder. Or it may 
dry and finally become calcified. 

Tubercular Inflammation. — This form of inflammation in the tubes 
is most frequently seen in its later stages, when the mucous membrane is 
partially or entirely converted into a thick, cheesy, often ulcerating 
layer. The lumen of the tubes may be dilated, the walls thickened from 
chronic inflammation. This lesion may occur by itself, or may be asso- 
ciated with tubercular inflammation of the lungs, or of the other genito- 
urinary organs, or the peritoneum. The lesion usually commences at 
the abdominal ends of the tubes, and both tubes are apt to be involved. 

Syphilitic Inflammation in the form of a diffuse thickening of the 
wall by gummatous tissue has been described. 

TUMORS. 

Small fibromata and fibro-myomata sometimes occur in the wall of 
the tubes or in the fimbriae. Small Upomata have been seen between 
the folds of the broad ligament in close connection with the tubes. 

Carcinoma of the tubes is usually, if not always, secondary to cancer 
of the uterus or ovaries. 

Cysts, usually of small size, sometimes pediculated and with thin 
walls, are frequently seen in the peritoneal covering of the tubes or in 
the fimbriae. They are believed to be of embryonal origin. 

KXTRA-UTERINE PREGNANCY. 

Tubal Pregnancy.— The impregnated ovum is in some way hindered 
from passing into the uterus, becomes fixed in the tube, and is there 
developed. The villi of the chorion grow into the mucous membrane of 
the tube, forming an incomplete placenta. Eare cases are recorded in 
which the placenta was situated in the uterus while the foetus was de- 
veloped in the tube. The embryo and its membranes are developed until 
they reach such a size that the tube surrounding them ruptures. This 
may occur in the first month or not until much later. In rare cases, 
when the wall of the tube was extensively involved in the formation of 
the placenta, the development has gone on until term. The ovum may 
remain in the tube after the rupture; or may escape into the peritoneal 



THE ORGANS OF GENERATION. 463 

cavity, still enveloped in its membranes; or the membranes may be rup- 
tured aud left in the tube. The rupture is generally attended with fatal 
haemorrhage. In some cases,, death is caused by the rupture of a dilated 
vein while the tube is still intact. Haemorrhage into the sac may occur 
before its rupture. 

In rare cases, death does not take place, and the foetus is shut in by 
adhesions and false membranes. The embryo soon dies. In favorable 
cases, there is a slow absorption of the soft parts of the foetus, the bones 
are separated and left imbedded in a mass of fibrous tissue, fat, chole- 
stearin, and pigment. Or the foetus retains its shape and becomes mum- 
mified, and may then be incrusted with the salts of lime. 

In unfavorable cases, degeneration and gangrene of the foetus take 
place rapidly, with inflammation and suppuration of the surrounding 
tissues. There may be perforation and escape of the broken-down foetus 
through the rectum, vagina, bladder, or abdominal wall. The patient 
may die from peritonitis or exhaustion, or may recover after the escape 
of the foetus. 

In some cases, the foetus may escape through a rupture of the tube 
into the space between the folds of the broad ligament. 

Tubo- abdominal Pregnancy is produced by the development of the 
ovum in the fimbriated extremity of the Fallopian tube Adhesions are 
formed, so that the foetus is partly in the end of the tube and partly in 
the abdomen. 

• Interstitial Pregnancy. — The ovum in these cases is arrested and 
developed in the portion of the tube which passes through the wall of the 
uterus. 

Abdominal Pregnancy. — The ovum, after escaping from the ovary, 
does not enter the Fallopian tube, but becomes fixed to the peritoneum, 
usually at some part near the ovary. It is surrounded by thickened peri- 
toneum and develops in that position. 

Ovarian Pregnancy. — The existence of this form of pregnancy is 
doubtful and difficult to prove, but there are some cases in which it 
seems probable that the ovum develops in its Graafian follicle. The pla- 
centa may be attached to the tube or to the abdominal wall. 

In all forms of extra-uterine pregnancy, the uterus becomes enlarged, 
and a sort of decidua is formed on its internal surface. 

LESIONS OF THE PLACENTA. 

Aside from the variations from the normal in size, shape, and posi- 
tion, for a description of which we refer to the works on obstetrics, we 
may briefly mention here some of the more important structural changes 
which the placenta may undergo. 

Hcemorrhage. — This may occur either on the maternal surface in the 
decidua; or between the foetal surface and the membranes; or in the 



464 THE ORGANS OF GENERATION. 

substance of the placenta. The latter form of haemorrhage constitutes 
the true placental apoplexy. This may occur as the result of rupture of 
a placental sinus. The placental tissue is crowded apart, and a blood- 
clot, often infiltrating the parenchyma, is formed. This may lead to 
abortion, or the blood may undergo disintegration and absorption, and 
its place be occupied by a cicatrix. The placental tissue in its vicinity 
may undergo fatty degeneration. Under other conditions, without evi- 
dence of rupture of the vessels, the placental tissue may become infil- 
trated with blood in the form of an infarction. In this, degenerative 
changes, similar to the above, may occur, leading to fibrous induration 
of the placenta. 

INFLAMMATION < (PLACENTITIS). 

Suppurative Inflammation of the placenta, with the formation of 
abscesses, is of rare occurrence as the result of injury. 

Chronic Indurative Inflammation of the placenta may result in the 
formation of circumscribed masses of cellular and loose, or dense and 
cicatricial connective tissue, or in a diffuse formation of connective 
tissue, which may interfere with the nutrition of the foetus and cause 
abortion. The new-formed connective tissue may undergo fatty degene- 
ration or calcification. 

In another class of cases, the new connective tissue is formed mainly 
in the walls of the vessels, particularly the arteries. This may occur 
in circumscribed portions of the vessels, leading to nodular growths 
around the arteries, or it may occur extensively along the various rami- 
fications of the vessels, converting them into thick fibrous cords. The 
change is primarily in the adventitia, but all the coats of the vessel may 
become involved, leading to more or less complete obliteration of the 
lumen. 

Various proliferative and indurative changes in the placenta may 
occur as the result of syphilitic infection. 

DEGENERATIONS. 

Fatty and amyloid degeneration and calcification of the placental tis- 
sue are of not infrequent occurrence. 

Cysts of the placenta are of occasional occurrence; their origin is in 
most cases obscure. 1 

THE MAMMA. 
MALFORMATIONS. 

Absence of both mammae is only found in connection with other 
marked malformations. 

1 See Ahlfeldt, Arch, fur Gynakologie, Bd. 2, p. 397. Fenomenodes, ibid., Bd. 
15, p. 343. 



THE ORGANS OF GENERATION. 465 

Absence of one mamma has been observed in a few cases, with and 
without defective development of the corresponding half of the thorax. 

Absence of one or of both nipples is more common. 

Arrest of development of the mammae is found in connection with 
arrest of development of the organs of generation, and, to a less degree, 
alone. 

Supernumerary mammae and nipples have been observed in a number 
of cases. The glands may all secrete milk during lactation. 

Too early development of the mammae is sometimes found in young 
children in connection with abnormal development of the organs of 
generation. 

HEMORRHAGE. 

In young women who surfer from amenorrhea or dysmenorrhea, 
small haemorrhages sometimes occur in the mammae at the time of men- 
struation. The blood may find its way into the milk ducts and exude 
in small quantities at the nipple. 

Contusions of the breast may produce extravasations of blood in the 
mammary gland or the surrounding connective tissue. This may be- 
come absorbed, or may remain and be surrounded by fibrous tissue or 
be converted into cysts. 

INFLAMMATION. 

During lactation, the nipple is liable to become inflamed in three 
ways, which may occur separately or be combined together. 

1. The epidermis is rubbed off by nursing, the cutis becomes in- 
flamed and converted into granulation tissue; in this way small or large 
ulcers may be formed. 

2. Fissures are formed at the base of the nipple, which extend com- 
pletely through the skin, and are lined at the bottom with granulation 
tissue. 

3. There is a diffuse inflammation of the whole nipple, which does 
not, however, go on to suppuration. The nipple is conical, red, swollen, 
and very painful. 

Acute Inflammation of the Mamma (Mastitis) occurs most frequently 
during lactation; it also occurs during pregnancy, and occasionally in 
women who are neither pregnant nor nursing. 

The inflammation may. involve the subcutaneous connective tissue, 
the gland itself, or the connective tissue between the gland and the wall 
of the thorax. The inflamed tissues are at first congested, swollen, hard, 
and painful. The inflammation may stop at this point and resolution 
take place; but more frequently it is succeeded by suppuration. If the 
inflammation involves the subcutaneous connective tissue, the abscess 
may be superficial and soon open through the skin. If the gland is 



±66 



THE ORGANS OF GENERATION. 



involved, one lobule after another may become inflamed (Fig. J 94), so that 
successive abscesses are formed in different parts of the gland. If the 
connective tissue beneath the gland is inflamed, a deep abscess of large 
size may be formed, which usually perforates through the skin, but 
sometimes into the pleural cavity. In both these latter forms of abscess 
there is apt to be necrosis of large portions of tissue. These abscesses 
may cicatrize, or they may pass into a chronic condition and remain as 
suppurating, fistulous tracts for a long time. 

In new-born children, there is often a painful swelling of the breasts, 
which usually subsides in a few days, but may go on to suppuration. 

Epidemic parotitis is sometimes complicated by mastitis. 




Fig 194.— Suppurative Mastitis occurring in the Non-functionating Gland. 
a, milk ducts; 6, interstitial tissue ; c, dense collections of pus ; d, diffuse infiltration of lobule 
with pus. 



Chronic Inflammation of the interstitial connective tissue of the 
mammary gland may result in the formation of dense connective tissue 
(Fig. 195), with or without cystic dilatation of the milk ducts and 
atrophy of the glandular elements. Acute exudative inflammation may 
occur in a gland which is the seat of chronic inflammation, and abscesses 
may be formed. 

Eczema sometimes affects the skin of the nipple. Attention has 
lately been drawn to the relationship between this inflammation and 



THE ORGANS OF GENERATION. 



467 



carcinoma of the nipple, for the two are frequently associated. It is 
possible that the eczema may lead to the subsequent development of the 
carcinoma. 

Syphilitic ulcers may occur in the nipple either as primary chan- 
cres or as mucous patches. Gummy tumors have been observed in the 
mamma. 

TUMORS. 

There may be a general hypertrophy of one or both breasts. This is 
usually found in young, unmarried women, but sometimes in advanced 
life. There is an increase in all the elements of the gland, both the 
glandular and the connective tissue. 

Cysts of the mamma seem to be for the most part retention cysts, 
formed by the dilatation of the glandular ducts or acini. During lacta- 








Fig. ITS.— Chronic Inflammation of Mammary Gland. 

tion, such retention cysts are sometimes formed, and then contain milk. 
They may reach an enormous size. At other times, retention cysts are 
formed containing serous or viscid brownish fluid, which often exudes 
through the nipple. These cysts may be large or small, single or mul- 
tiple. There is usually at the same time some growth and induration 
of the connective tissue of the gland. In some cases there are polypoid 
outgrowths of connective tissue from the wall of the cyst. These cysts 
are not to be confounded with the cysts which are developed with the 
intracanalicular tumors, of which we shall speak below. 

Fibroma. — Circumscribed tumors composed of connective tissue are 
sometimes found in the breast. They are dense and hard, and may 
inclose in them some of the glaud ducts and acini. 

Intracanalicular Fibroma. — These tumors are formed by a diffuse 
growth of connective tissue, a dilatation of the milk ducts, and a growth 
of polypoid fibrous tumors from the walls of the ducts into their cavi- 



468 



THE ORGANS OF GENERATION. 



ties. The glandular acini may be atrophied, or enlarged, or cystic. A 
section of such a tumor looks like a solid mass of fibrous tissue, divided 
by clefts and fissures lined with cylindrical or cuboidal epithelium (Fig. 
196), or containing cysts into which project polypoid fibrous outgrowths. 
These tumors grow slowly, but if left to themselves may reach an enor- 
mous size. The skin over them may ulcerate and the tumor project 
through the opening in fungous masses. 




lllll 



1 




^ 



^s 



swassts 




g^fiw*^s|^ 



Fig. 196.— Intracanalicular Fibroma op the Mamma, x 170 and reduced. 
Cross-section of a milk duct with polypoid ingrowths. * 

Sometimes the new connective tissue forms a more or less thick 
cylindrical investment of the duct without growing into its lumen. 
This formation, which is shown in Fig. 197, is sometimes called peri- 
canalicular fibroma. 

Myxoma. — This form of tumor may occur as a circumscribed growth 
replacing part of the mamma; or it may be developed in the same way 
.as the intracanalicular fibromata. It is not uncommon in these intra- 



THE ORGANS OF GENERATION. 



469 



canalicular tumors to find a combination of fibrous, mucous, and sarco- 
matous tissue in the same tumor. 

Chondroma is a very rare form of tumor in the mamma. A few cases 
have been described in which it was combined with carcinoma. 

Adenoma. — Tumors composed of glandular acini, and ducts sur- 
rounded by connective tissue, are of frequent occurrence in the mamma 
(Fig. 68, page 148). They are either single or multiple, or several may 
be developed successively in the same breast. They grow at first slowly, 
afterwards more rapidly. Their structure may be further complicated 
by the dilatation of one or more of the ducts which compose the tumor 
into cysts, and the ingrowth of connective tissue from the walls of these 
cysts. 

Sarcoma. — This form of growth may be developed as a circumscribed 




Fig. 197. — Pericanalicular Fibroma of the Mamma. 

tumor of small or large size. Its basement substance is that of connec- 
tive or of mucous tissue, and may be scanty or abundant. The cells are 
spheroidal, fusiform, branched, or polygonal. These tumors may simply 
replace the gland; or glandular acini and ducts may be inclosed within 
them ; or these ducts and acini may be dilated so as to form cysts; or there 
may be a new growth of the gland tissue so as to form an adeno-sarcoma. 

In other cases the sarcoma takes the intracanalicular form. There 
is a diffuse growth of sarcomatous tissue, a dilatation of milk ducts, and 
an outgrowth of sarcomatous tissue from the walls of the dilated ducts 
into their cavities. These tumors often reach an enormous size, and 
there is apt to be ulceration of the skin over them. 

Carcinoma of the mamma is most common in women between the 



470 THE ORGANS OF GENERATION. 

ages of thirty-five and fifty-five, but it sometimes occurs in women not 
over twenty years old, and sometimes in old persons. It occurs in either 
breast, in the right rather more frequently than in the left, but some- 
times in both. The growth begins more frequently at the periphery of 
the gland than at its centre, and more frequently in the upper edge of 
the gland than in any other place. 

The growth most frequently begins as a small, circumscribed nodule, 
which enlarges and involves more and more of the breast; sometimes, how- 
ever, it is diffuse from the first, and sometimes it begins in the nipple. 

It may infiltrate the adjacent tissues and the axillary and cervical 
glands, and form metastatic tumors in different parts of the body. 

There are several different anatomical forms of the growth: 

1. Those in which the epithelial elements preponderate, the soft or 
so-called medullary carcinomata. 

2. Those in which both the connective-tissue stroma and the epi- 
thelial cells are both prominently developed, the cells lying in well- 
defined larger and smaller irregular-shaped spaces, so that the simulation 
of gland tissue is tolerably close. These are called carcinoma simplex. 

3. The tumors in which the connective-tissue stroma preponderates, 
giving the tumor its hard, dense character. This is the carcinoma 
fibrosum, or scirrhous. 

Colloid carcinoma of the mamma is rare. Various secondary changes 
may occur in these tumors, such as have been described in the section on 
Tumors. 

In any of these forms of cancer there may be cystic dilatations of the 
ducts and acini. 

Besides the primary cancers of the mamma, secondary cancers are 
met with in rare cases. 

MALE. 

THE PENIS. 

MALFORMATIONS. 

Entire absence of the penis is met with in connection with great de- 
fects of development of the rest of the body. 

Absence of the penis, with proper development of the other organs of 
generation, is rare. The urethra then usually opens into the rectum. 

An abnormally small penis is found with absence or arrested develop- 
ment of the testicles. 

Absence or a rudimentary form of the prepuce has been observed in 
a number of cases. Congenital phimosis is also not infrequent. 

Hypospadia consists in an arrest of development of the penis and 
scrotum. In its highest degrees, the penis is one-half to one inch long, 
the glans penis small and resembling a clitoris. On the lower side of 






THE ORGANS OF GENERATION. 471 

the penis is a deep cleft lined with mucous membrane. Into this cleft 
the urethra opens at the root of the penis. The scrotum remains sepa- 
rated into two halves, resembling labia majora. The testes descend into 
their proper position on each side or remain in the abdomen. If the 
testicles continue to develop normally, the individual has the appearance 
and capacities of a man; if their development is arrested, the individual 
is small and has a womanish appearance. 

In lesser grades of the same malformation, the two halves of the scro- 
tum are joined and the penis is larger, but a part of the urethra remains 
open as a cleft at any point of the penis. 

Epispadia is an opening of the urethra on the upper side of the penis. 
It presents various grades and forms. 

Hermaphroditism. — This is a union of two sexes in the same person, 
the test of which is the presence of the secreting organs, the ovaries, and 
testicles. True hermaphroditism is rare, but it does occur, while most 
of the conditions called hermaphroditism are in reality due to varying 
malformations of the external generative organs. 

Pseudo-hermaphroditism. — This malformation consists in an abnor- 
mal change in the transition from the foetal condition of the parts to 
their fully developed form. In the male, normally, the greater part of 
Miiller's canal disappears, and its lower end forms the vesiculaprostatica. 
In this malformation, Miiller's canal is changed, as it is in the female, 
into Fallopian tubes, uterus, and vagina, while at the same time the 
testes, epididymes, vesiculae seminales, and spermatic cord are formed 
as usual. In the. lesser degrees of this malformation, we find, in the 
place of the vesicula prostatica, a pear-shaped sac as large as a pigeon's 
egg, with muscular walls and an epithelial lining. This sac may be 
incompletely divided into a uterus and vagina, and it opens into the 
urethra. In the higher grades, we find a well-formed vagina and uterus. 
The uterus may or may not have Fallopian tubes. The testicles are 
usually retained in the abdomen or inguinal canals, and are small. The 
spermatic ducts run on the sides of the uterus and open into the ure- 
thra or are closed. The penis and scrotum appear as in hypospadia, 
or are well formed. The appearance of the individual varies with the 
development of the testicles. 

True Hermaphroditism may be lateral. In this condition there is 
hypospadia; a vagina and uterus and a Fallopian tube and ovary on one 
side, and a testicle and spermatic cord on the other. 

In certain cases, which may be called bilateral hermaphroditism , 
there is a testicle on one side and an ovary on the other. 1 

1 For a detailed consideration of the malformations of the male and female gene- 
rative organs, consult Klebs, " Handbuch der pathologischen Anatomie," and more 
recent cases of hermaphroditism by Heppner, Arch. f. Anat. u. Physiol., 1870, and 
by Hofmann, Wien. Med. Jahrb., 1877. 



472 THE ORGANS OF GENERATION. 

Enlargement of the penis is sometimes caused by venous congestion 
from heart disease; by long-continued masturbation, as a result of which 
the corpus cavernosum may lose its contractility; and in rare cases by 
hypertrophy of the stroma of the corpus cavernosum. 

Injury and Hemorrhage. — Injuries to the penis are liable to give 
rise to severe haemorrhage on account of its peculiar vascular character; 
suppurative inflammation, gangrene, infiltration with urine and its con- 
sequences, are also liable to occur. The contractions of the cicatricial 
tissue by which wounds are healed frequently give rise to various dis- 
tortions of the organ and not infrequently prevent subsequent erections. 

INFLAMMATION. 

Balanitis, inflammation of the prepuce, is usually produced by gonor- 
rhoea or by accumulations of smegma. The skin is red and swollen 
and may ulcerate. Condylomata may be formed, and adhesions between 
the prepuce and glans. The glans may ulcerate and the prepuce maybe 
much thickened. If the prepuce is long, there is an inflammatory 
phimosis, and the products of inflammation accumulate within the swol- 
len prepuce. In some cases, the prepuce becomes gangrenous. 

Paraphimosis is produced by the retraction of a narrow prepuce be- 
hind the glans, with consequent stricture, inflammation, and sometimes 
gangrene. 

Inflammation of the Corpora Cavernosa is produced by gonorrhoea, 
injuries, fistulae, typhus fever, measles, and occurs in connection with 
inflammation of the connective tissue of the pelvis. It results in fibrous 
induration of portions of the corpora cavernosa; in rare cases, in ab- 
scesses or diffuse purulent infiltration; sometimes in gangrene. 

Syphilitic Ulcers frequently occur on the glans penis and prepuce. 
The indurated chancre is formed either from an excoriation in which a 
pustule is formed or from a little nodule. The pustule breaks and its 
walls are infiltrated with small round cells. The nodule softens, breaks 
down, and forms an ulcer, of which the walls are infiltrated with cells in 
the same way. 

Syphilitic condylomata are of frequent occurrence on the glans. 

Phagedaenic ulcers occur and may destroy a considerable part of the 
penis. Herpes of the prepuce occurs in the form of small vesicles, which 
may later become ulcers. Erysipelatous and furuncular inflammation 
sometimes involve the skin of the penis. 

TUMORS. 

Papilloma is found on the prepuce and glans penis. It occurs in the 
form of little warty growths, or of composite, cauliflower masses, even 
as large as a fist. In either case, the structure is the same, hypertrophied 



THE ORGANS OF GENERATION. 473 

papillae covered with epithelium. Sometimes the epithelial layers be- 
come thick and horny, forming large, dense projections. 

Fibroma diffusiim, or elephantiasis of the prepuce, may occur, lead- 
ing to immense thickening of the structure. It consists in a diffuse 
growth of the deep fibrous tissue of the cutis. Lipomata, angiomata, 
circumscribed fibromata, and sebaceous cysts may occur in the penis. 
Carcinoma of the penis usually occurs in the form of epitheliomata. 
These are most frequent in the prepuce and glans penis. They may have 
the form of flat ulcers, or of infiltrating, ulcerating nodules, or very fre- 
quently assume the form of papillary outgrowths, which may attain great 
size, ulcerate, or undergo a variety of inflammatory changes. These 
growths may involve the entire skin of the penis; they may invade 
deeper parts. The inguinal glands maybe invaded. Distant metastases 
may occur, but are not frequent. 

Glandular carcinoma of the penis is not common. It may be secon- 
dary to carcinoma in some other part of the body. 

Calcification and Ossification of the connective tissue of the corpora 
cavernosa sometimes occur. Large and small preputial calculi are occa- 
sionally found between the prepuce and the glans. These may be 
formed in situ, may come from the bladder or from without, and may 
later increase in size. 

THE SCROTUM, 

The skin of the scrotum is subject to the various forms of lesions 
which may occur in any part of the integument. 

Elephantiasis of the scrotum consists in the main of a development 
of new connective tissue from the cutis, which is sometimes accompanied 
by dilatation of the lymph vessels. The thickened scrotum sometimes 
forms very large tumors, often rough upon the surface, which may en- 
tirely cover in the penis. Lip miat a, fibromata, atheromatous or sebaceous 
cysts, and dermoid cysts containing hair, bone, cartilage, etc., are some- 
times found. Occasionally the skin of the scrotum is beset with numer- 
ous larger and smaller sebaceous cysts, which raise the surface into little 
wart-like projections. Epitheliomata, in the form of flat or papillary 
ulcerating tumors, are of frequent occurrence among chimney sweepers, 
and may lead to extensive ulcerations of the adjaceut parts and involve- 
ment of neighboring lymph nodes. 

In very rare cases, tumors containing a considerable portiou of a fceta) 
skeleton have been found in the scrotum. 
38 



474 THE ORGANS OF GENERATION. 

THE TESTICLES. 
MALFORMATIONS. 

Absence of both testicles, either with or without absence of the epi- 
didymes, spermatic cords, and vesiculse seminales, occurs in rare cases. 
The scrotum is only indicated or may contain the epididymes. The 
penis is small, and the individuals are small and poorly developed. 

Instead of being entirely wanting, the testes may be imperfectly 
developed. The individuals are weakly and effeminate. Absence of one 
testicle, with healthy development of the other, is more frequent. The 
corresponding epididymis and cord may be absent or present. 

The spermatic cords and vesiculae seminales may be absent or imper- 
fectly developed on one or both sides, while the testes are normal. 

Either one or both testicles may remain permanently in their foetal 
position, or may not descend into the scrotum for several years after 
birth (crypt or chismus). Their descent may even be delayed until the 
thirtieth year of life. This condition may depend on an arrest of de- 
velopment in the testes or the gubernaculum testis ; on adhesions pro- 
duced by intra-uterine peritonitis ; on narrowing of the inguinal canal ; 
on narrowing or shortening of the vaginal process of the peritoneum; or 
on abnormal size or position of the testicle. Usually the malformation 
is confined to one testicle, and then is more frequent on the left side. 
The testicle is usually found in the abdomen close to the mouth of the 
inguinal canal, or in the inguinal canal just below the external ring; but 
it may be beneath the skin in the perineum, or in the crural canal with 
the femoral vessels, or elsewhere. The retained testis is usually not fully 
developed, or undergoes fatty or fibrous degeneration. The retention of 
one or even of both testicles does not preclude the possibility of procrea- 
tion. Eetained testicles are prone to inflammatory changes and liable to 
become the seat of malignant tumors. 

Sometimes, while the testis is retained, the epididymis and spermatic 
cord descend into the scrotum. In rare cases, the position of the testis 
may be changed, so that the epididymis and cord are in front. The ex- 
istence of a supernumerary testis has been asserted in some cases, but is 
rather doubtful. 

Atrophy of the testicle may occur in old age or in persons who are in 
a condition of premature senility ; or as the result of pressure from 
hernise, hydrocele, or inflammatory products. 

HYDROCELE. 

Hydrocele of the tunica vaginalis consists in an accumulation of serum 
in the cavity of this membrane. It is usually confined to one side. It is 
caused by acute or chronic inflammation of the tunica vaginalis, by vari- 
cocele, or by general dropsy. The serum is found in small or in large 



THE ORGANS OF GENERATION. 475 

quantities; it is usually transparent, may contain cholestearin, or be 
purulent and contain the pyogenic bacteria, or be mixed with blood. 
The tunica vaginalis remains unchanged, or is thickened, or contains 
plates of bone, or is covered with polypoid fibrous bodies, which fall off 
and are found free in the cavity of the sac. There may be adhesions 
between the layers of the tunica vaginalis, and in this way the fluid be- 
comes sacculated. The testis is pushed downward and backward ; it 
remains unchanged or is atrophied. 

Hydrocele of the processus vaginalis consists in an accumulation of 
serum in the cavity of the vaginal process of the peritoneum, which re- 
mains open after the descent of the testicle. There are several different 
varieties. 

(a) The vaginal process is entirely open, and there is a free commu- 
nication with the peritoneal cavity. The serum may originate in the 
cavity of the peritoneum or of the vaginal process, and passes freely from 
one to the other. 

(b) The processus vaginalis is closed in the inguinal canal while its 
lower portion is filled with serum. 

(c) The processus vaginalis is closed about the testis, and the visceral 
layer of the tunica vaginalis is formed. The serum accumulates in the 
upper part of the vaginal process, which communicates with the peri- 
toneal cavity. 

(d) The vaginal process is closed in the inguinal canal and over the 
testis; the serum accumulates so as to form one or more sacs between 
these two points. Inguinal hernia may complicate this form of hydro- 
cele. 

Hydrocele of the spermatic cord consists in a general oedema of the 
connective tissue of the cord, or in the development of circumscribed 
cysts in this connective tissue. 

A peculiar form of hydrocele is produced by the accumulation of 
serum in the sac of an inguinal hernia, from which the intestine has be- 
come retracted. 

SPERMATOCELE. 

Cysts containing spermatic fluid not infrequently arise from the epi- 
didymis or from the rete testis. These sometimes acquire a large size 
and crowd the tunica vaginalis before them, so that they simulate a col- 
lection of fluid in the cavity of the latter. The wall of the cyst may be 
lined with ciliated or with flattened epithelium. The contents are some- 
times simply serous, but more frequently opalescent and contain great 
numbers of spermatozoa. 

HEMATOCELE. 

Hematocele of the tunica vaginalis consists in an effusion of blood 
into the cavity of this sac. It may be produced by injury; in scurvy, or 



476 THE ORGANS OF GENERATION. 

the hemorrhagic diathesis; or it may complicate a pre-existing hydrocele. 
The effused blood usually soon degenerates, and we find the sac filled 
with a brownish fluid or a thick, grumous mass. The tunica vaginalis 
may be thickened. The testis remains normal or is atrophied. 

Effusion of blood into the loose connective tissue of the scrotum is 
often called extravaginal hcematocele. 

Hematocele of the spermatic cord occurs in rare cases as a diffused 
infiltration of blood in the connective tissue of the cord. Or blood may 
be effused into a hydrocele of the cord. 

INFLAMMATION. 

Inflammation of the testicles may be caused by injuries, exposure to 
cold, inflammation of the urethra, syphilis; or it may occur in parotitis. 
The testes, epididymis, or tunica albuginea may be principally involved. 
Usually only one testicle is inflamed, sometimes both. The inflamma- 
tion may extend to the vas deferens. The inflammation may be acute 
or chronic. 

Acute Orchitis is most frequent in the epididymis and tunica albugi- 
nea. When the testis is involved, the organ is congested and infiltrated 
with serum or pus. From this condition it may return to the normal 
state, or small abscesses may form which may be absorbed, or they 
may increase in size so as to involve nearly the entire organ. They may 
perforate externally, and then healing may occur by means of granulation 
tissue; or extensive gangrenous destruction of the scrotum may occur. 
They may become inclosed in a fibrous capsule, and the contents dry and 
become cheesy or calcified, and so persist for a longtime. The acute in- 
flammation may pass over into the chronic form. Acute epididymitis is 
frequently the result of gonorrhceal infection, and may or may not be 
associated with inflammation of the testis. 

The products of inflammation may collect in varying quantity in the 
lumina of the seminiferous tubules, and in the ducts of the epididymis, 
and the epithelium of these structures may degenerate. 

Chronic Orchitis occurs as a sequel of acute inflammation or as an 
original condition. It may affect the testis, the epididymis, or the sper- 
matic cord. The seminiferous tubules may be filled with desquamated 
and degenerated epithelium; they may be atrophied, or their walls may 
be greatly thickened so that they are converted into dense fibrous cords, 
with almost or quite complete obliteration of their lumina. There is 
usually a marked increase in the interstitial tissue, which causes atrophy 
of the tubules (Fig. 198). The albuginea may be greatly thickened. 
In some cases, the testis is converted into a mass of dense connective tissue, 
in which but little trace of the original structure can be made out. The 
new-formed connective tissue may become calcified. A periorchitis may 



THE ORGANS OF GENERATION. 



477 



lead to thickening and union of the layers of the tunica vaginalis testis. 
Abscesses are not infrequent in connection with chronic orchitis. 

Tubercular Orchitis may occur in connection with tuberculosis of 
the other genito-urinary organs or the lungs, in acute general miliary 
tuberculosis, or by itself. It usually begins in the epididymis, and may 
extend from there to the testis; or it may commence in the testis itself. 
The appearances which the testicles present when the seat of this form 
of inflammation are exceedingly varied and difficult of interpretation. 
This is partly due to the complex structure of the organ, partly to the 
varied complicating simple inflammatory changes which the different 



-r^'Vy^; 



mmmK 



wmm Iff? 

'm&mMmmmm 



1 







\\kW 



mm 

■if Mm 



Fig. 198.— Chronic Interstitial Orchitis with Atrophy of the Seminiferous Tubules. 
a, thickened interstitial tissue; c, thickened membrana propria of the tubules; d, separated 
epithelial cell mass in the lumen of the tubules. 

parts of the organ undergo in connection with the special tubercular in- 
flammation, and the impossibility of making any definite morphological 
distinction between them. Further researches are urgently needed in 
this direction, and it seems probable that in the presence or absence of 
the tubercle bacillus we shall find the needed differentiating factor be- 
tween various inflammatory processes which are at present grouped 
under the general heading of tuberculosis testis. 

We may find in the testicle small circumscribed masses of cells, visible 



478 THE ORGANS OF GENERATION. 

to the naked eye as whitish spots, which are sometimes composed of 
small spheroidal cells or of larger polyhedral or fusiform or round cells. 
These occur in the walls of seminiferous tubules and blood-vessels and 
in the interstitial tissue. Sometimes associated with these smaller 
nodules, and sometimes not. we find larger, irregular yellowish or gray 
cheesy masses, which are believed by many to be formed by the conflu- 
ence and degeneration of the smaller nodules. The cheesy masses may 
break down and open externally, giving rise to fistulas, gangrenous in- 
flammation, etc. Hand-in-hand with this nodular formation of tissue, 
which is disposed to degenerative changes, there are various more or less 
diffuse alterations of the parenchyma and interstitial tissue of the organ 
which must not be overlooked, and which often constitute a most prom- 
inent and important factor in the lesion. The interstitial tissue may be 



a. f 9; 










Fig. 199.— Chronic Orchitis with the Formation of Structures resembling Miliary Tubercles. 
a, thickened interstitial tissue; 6, mass of granular cells in the interstitial tissue; c, thickened 
membrana propria of seminiferous tubule; d, mass of separated epithelium in tubule; e, accumula- 
tion of small spheroidal cells around tubules; /, thickened membrana propria inclosing g, a multi- 
nuclear mass resembling a giant cell. 



more or less densely and diffusely infiltrated with small spheroidal cells. 
The arteries are often the seat of obliterating endarteritis. The walls of 
the seminiferous tubules may be very much thickened, so that the lumen 
may be entirely obliterated. The epithelium lining the tubules may be 
fatty, disintegrated, and peeled off, or it may have largely disappeared. 
The lumen of the tubules may be filled with a granular, nucleated mass 
which in transverse sections looks like a giant cell. The thickened walls 
of the tubules may be infiltrated with small spheroidal cells, so that the 
underlying stroma is scarcely visible. When this occurs in connection 
with a similar infiltration of the interstitial tissue and the formation of 
giant cells in the lumina, we have structures which present the greatest 
resemblance to some forms of tubercle granula (Fig. 199). 



THE ORGANS OF GENERATION. 479 

Tubercular inflammation may extend from the testis to the vas de- 
ferens, vesiculse seminales, and prostate. 1 

Syphilitic Orchitis. — This may occur in the form of a diffuse new 
formation of connective tissue, which may occur in some particular part 
of the organ or be widely distributed through it, and by reason of which 
the organ becomes dense and firm. Morphologically, there is no differ- 
ence between this form of orchitis and chronic indurative orchitis from 
other causes. It may occur in children affected with congenital syphilis. 

G-ummata may form in connection with the interstitial induration. 
These may disappear, leaving irregular cicatrices. 

TUMORS. 

Fibroma occurs in the form of small dendritic or polypoid growths 
of the visceral layer of the tunica vaginalis. These sometimes become 
free, and are found in the sac, usually in connection with hydrocele. 
Small nodular fibromata occasionally occur in the albuginea and in the 
spermatic cord. 

Lipomata, either pure or in combination with myxoma and sarcoma, 
may arise from the connective tissue of the spermatic cord, or from the 
tunica albuginea. 

Chondroma, sometimes in a pure form, but more frequently combined 
with myxoma and sarcoma, occur in the testicles, and may attain a large 
size. Osteoma has been described. 

Sarcomata occur in the testes and epididymis, most frequently in the 
former. They present the greatest variety in structure. They may be 
composed of spheroidal or spindle-shaped cells; they may be soft or con- 
tain much fibrous tissue; they are very frequently combined with 
myxoma, chondroma, lipoma, etc. Owing to the occlusion of the semi- 
niferous tubules, cysts may be formed in these sarcomata. In these 
cysts polypoid growths of sarcomatous tissue may occur in the form of 
intracanalicular growths. Thus the so-called cysto-sarcomata of the 
testicle are formed. The walls of these cysts may coalesce, so that large, 
irregular cavities may be formed. When the cysts are not filled by poly- 
poid outgrowths from their walls, they may contain a mucous, serous, 
or bloody fluid, or masses of flattened cells, fat, and cholestearin. The 
cysts may be lined with cylindrical, ciliated, or flattened cells. 

Rhabdomyomata have been several times observed, frequently in com- 
bination with cysts. 

Adenoma is occasionally found, usually in combination with sarcoma, 
or carcinoma, or with cyst formation. 

1 For the literature of tuberculosis of the testicle consult Waldstein, " Zur Kennt- 
niss der tuberculosen Erkrankuagen des Hodens." Virch. Arch., Bd 85, p. 337, 

1881. 



480 THE ORGANS OF GENERATION. 

Carcinoma of the testicle is commonly of the soft medullary form, 
of rapid growth, and usually primary. It may commence in the testis 
or epididymis. Usually only one testicle is involved. Frequently the 
entire glandular portion of the organs is replaced by the new growth. 
The albuginea expands with the growth of the tumor, and may continue 
to inclose it even when of large size. The tissues are often very vascular, 
and haemorrhages, areas of softening, fatty and mucous degeneration are 
frequent. The inguinal and lumbar lymph nodes are apt to become in- 
volved, and distant metastasis may occur. Rarely the growth as- 
sumes a scirrhous form. 

Cysts. — Aside from the above-mentioned cysts which occur in con- 
nection with tumors and spermatocele, cysts may be formed from per- 
sistent remnants of Muller's canal in the epididymis, or from obstruction 
of the seminiferous tubules or ducts by inflammatory products or tissue. 

Dermoid Cysts of various kinds are of infrequent occurrence, and are 
sometimes quite complex in character. They may be imbedded in the 
substance of the gland. Probably some of the above-mentioned cystic 
rhabdomyomata belong here. 

parasites. 
Ecliinococcus may occur in the testis or epididymis. 

THE SEMINAL VESICLES. 

The seminal vesicles may be the seat of acute or chronic inflamma- 
tion, which is most frequently connected with inflammatory changes in 
adjacent parts, prostate, urethra, etc. As a result of chronic inflamma- 
tion, the vesicles may be atrophied, or they may be greatly dilated as a 
result of constriction of the ducts. 

Tubercular inflammation is usually secondary. Carcinoma of the 
rectum or other genito-urinary organs may secondarily involve the semi- 
nal vesicles. Small concretions, sometimes containing masses of sperma- 
tozoa, are occasionally found in the seminal vesicles. 

THE PROSTATE. 

Hypertrophy of the prostate is a frequent senile change; it is general 
or partial. 

In general hypertrophy, the entire organ is enlarged, and may reach 
the size of a man's fist. The enlargement is symmetrical, or is most 
marked in one half or in the so-called middle lobe. The organ is hard 
and dense, or soft or alveolar, containing numerous small openings from 
which a turbid fluid exudes. These different appearances depend upon 
the character of the hypertrophy. The muscular and fibrous tissue alone 
may be increased, which is most common, or at the same time the glan- 



THE ORGANS OF GENERATION. 481 

dular tissue, or the glandular tissue alone. In the latter case, the lesion 
is more properly an adenoma. The increase of muscular tissue properly 
constitutes a myoma. 

In partial hypertrophy, we find circumscribed nodules of muscular 
tissue or of muscular and glandular tissue. They are usually situated 
at the periphery of the organ and project into the bladder. They may 
become detached from the prostate, and are found as small, movable 
tumors beneath the mucous membrane of the bladder, 

Both forms of hypertrophy frequently produce, by pressure, reten- 
tion of urine and changes in the bladder. 

Atrophy of the prostate is sometimes seen in connection with atrophy 
of the testicles, with castration, and as a result of inflammation. Some- 
times the ducts of the glandular portion are enlarged, or there may be 
fibrous degeneration of the organ. 

INFLAMMATION. 

Inflammation of the prostate is caused by gonorrhoea, by injuries, or, 
more rarely, is idiopathic. It may run an acute or chronic course. The 
gland may after a time return to its normal condition, or is gradually 
converted into a mass of fibrous tissue filled with abscesses. The ab- 
scesses may perforate into the bladder, urethra, vesiculse seminales, rec- 
tum, or peritoneum. Or the inflammation may extend to the connec- 
tive tissue of the scrotum or beneath the pelvic peritoneum. The pus 
may become thickened and cheesy, or even calcified. 

Tubercular Inflammation of the prostate usually accompanies a simi- 
lar lesion of some of the other genito-urinary organs, and is rarely of 
primary occurrence. Large cheesy masses are often formed, which may 
break down and open into the bladder or rectum. 

TUMORS. 

Adenoma of the prostate occurs in one of the forms of hypertrophy 
of the gland, either with or without an increase in the fibro-muscular 
interstitial tissue. 

Carcinoma is of occasional occurrence, and may be primary or 
secondary. 

Cysts of the prostate are sometimes found either as a result of occlu- 
sion of the ducts by hypertrophy of the interstitial tissue, tumors, etc., 
or as a result of faulty development. 

PARASITES. 

Ecliinococcus of the prostate has been described, but is rare. 

CONCRETIONS. 

Small ovoidal or spheroidal bodies having the characters of corpora 
amylacea are of very frequent occurrence in the alveoli of the prostate, 



482 THE ORGANS OF GENERATION. 

particularly in old persons. We find a certain number of them in the 
prostate of nearly all old men, but they are sometimes present in great 
numbers. Larger, irregular concretions, apparently formed by the co- 
alescence or growth of the smaller ones, are less frequently found, and 
may be incrusted with lime salts. These concretions may give rise to 
ulceration of the ducts of the gland or to interference with the passage 
of urine, but in a majority of cases they seem to be of little or no prac- 
tical importance. 

THE MALE MAMMA 

There may be an abnormal number of mamma?. In boys, at about 
the time of puberty, the mammae may be swollen and inflamed, or they 
may secrete milk. Cases are recorded in which adult males possessed 
large mammae which secreted milk. The breasts may be enlarged from 
an increase of fat or of connective tissue. 

Cysts of the male breast are not very infrequent. Fibromata, sarco- 
mata, cysto- sarcomata, myxomata, and various forms of carcinomata are 
recorded. 1 

'For literature of tumor of male mamma, see Gross, " Tumors of the Mammary 
Gland," p. 237. 



THE BO^ES. 



DISTURBANCES OF CIRCULATION. 



Hypercemia. — The evidences of this condition are most marked to 
the naked eye in the periosteum and marrow, particularly the latter. 
It should be remembered that the color of the marrow varies consider- 
ably under normal conditions, depending upon age and situation. In 
the bones of the foetus and new-born, and near the areas of ossification 
in the young, the marrow is normally, red in color. In adults, the mar- 
row of the sternum, vertebrae, and to a certain degree that of the ribs, 
pelvic and cranial bones, and the cancellous tissue of the ends of the 
long bones, is red or reddish in color. But most of the marrow, par- 
ticularly in long bones of the extremities, is of a yellowish color from 
the presence of fat cells. In old age the marrow of all the bones is apt 
to become pale, and to assume a more or less translucent or gelatinous 
appearance. 

Hyperemia usually occurs as an accompaniment of inflammatory 
processes in the bone, and, when marked, the periosteum is swollen and 
red; the compact bone tissue may appear of a pink color, while the mar- 
row, either by an increase in the amount of blood or absorption of 
its fat, or both, may be of a uniform dark-red color, or mottled with red 
and reddish yellow. 

Haemorrhage. — This may be due to wounds and injuries, to inflam- 
matory and necrotic processes; and small haemorrhages often accompany 
scurvy, purpura, haemorrhagic diathesis, and leukaemia. Haemorrhages 
of considerable size between the periosteum and bone may lead to seri- 
ous consequences, by cutting off the blood-supply to the superficial layers 
of bone, and thus inducing necrosis; but when not in contact with the 
air, they are not usually of serious import, since they are readily ab- 
sorbed. The smaller haemorrhages of the medulla are not usually of 
much importance. The decomposition of the extravasated blood may 
lead to extensive pigmentation of the marrow. 

WOUNDS, FRACTURES, AND DISLOCATIONS. 

For details of the varied alterations produced under these conditions, 
and the secondary changes involved in the healing process, we refer to 



484 THE BONES. 

the works on surgery. It may be stated here, however, that the healing 
of fractures occurs by the formation of granulation tissue in greater or 
less amount about the seat of fracture, and the direct formation of bone 
under the influence of osteoblasts, or by a preliminary formation of car- 
tilage or fibrous tissue and the gradual conversion of this into bone by 
metaplasia. 

INFLAMMATION. 

The periosteum, bone tissue, and marrow are so intimately connected 
that in most cases they all share to a greater or less degree in the patho- 
logical alterations of the bones. But as sometimes one, sometimes 
another is most markedly involved, it is convenient to consider sepa- 
rately here the inflammatory changes by which they are respectively 
affected. 

Periostitis. 

We may distinguish several varieties : 

1. Simple Acute Periostitis. — This form is apt to occur in children 
and ill-nourished persons from comparatively slight injuries or from 
unknown causes. The periosteum is thickened, succulent, congested, 
and more or less abundantly infiltrated with leucocytes, while the con- 
nective-tissue fibres are swollen. The periosteum becomes less firmly 
adherent to the bone, and the cells of the inner layers are increased in 
number. This variety of inflammation may terminate in the disappear- 
ance of the new elements and complete resolution ; or it may represent 
a preliminary stage of one of the other varieties of inflammation. 

2. Suppurative Periostitis may begin as a simple or as a purulent 
inflammation. The pus is formed in the inner layers of the periosteum, 
and between it and the bone. The outer layers of the periosteum may 
resist for a long time the suppurative process. The accumulation of pus 
may dissect up the membrane from the bone and leave the latter bare. 
The pus thus formed may remain in this position for a long time, may 
be absorbed, may become dry and cheesy, or may burst through the peri- 
osteum and form abscesses in the soft parts. The bone, if separated 
from its nutrient membrane, may remain unchanged, but more fre- 
quently necrosis, or inflammation of the bone itself, is set up. Such a 
periostitis may run an acute or a chronic course. 

Sometimes suppurative periostitis takes on a very malignant charac- 
ter. Pus is developed not only beneath but in the periosteum, forming 
abscesses filled with foul pus. The periosteum breaks down into a gan- 
grenous foul-smelling mass, and the same change may affect the neigh- 
boring soft parts. The medulla may take part in the process and break 
down into a purulent, gangrenous mass. Haemorrhages may complicate 
the process. The lymphatic nodes are enlarged and swollen ; abscesses 
may form in different parts of the body, and the patient may die with 



THE BONES. 485 

the symptoms of septicaemia. The pyogenic cocci may be found, under 
these conditions, in the exudations of the periosteum as well as in the 
metastatic abscesses. 

3. Fibrous Periostitis. — This is a low, chronic form of inflammation, 
resulting in the formation of new connective tissue in the periosteum, 
which becomes thickened and dense and unusually adherent to the bone. 
It may be the result of necrosis, chronic arthritis, chronic ulcers of ad- 
jacent soft parts, etc. It may follow a simple acute periostitis. 

4. Ossifying Periostitis results in the formation of new bone from 
the inner layers of the periosteum. The masses of new- formed bone, 
called osteophytes, are of variable shape. They may form a thin, velvet- 
like, villous layer; or they are little spiculae; or they form larger, rounded 
masses, or a thick, uniform layer, extending over a large part of a bone. 
They may be at first very loosely connected with the bone. The new 
bone has at first a loose, spongy character. It is formed of thin plates 
of bone inclosing large cavities filled with marrow. Layers of compact 
bone tissue are formed from the medulla on the sides of the original 
plates, and thus the medullary cavities are gradually filled up with bone. 
The new bone may thus become as compact or even denser than normal 
bone. The hyperostoses and exostoses thus formed may remain indefi- 
nitely, or they may gradually become smaller and finally disappear by 
absorption. 

The formation of new bone in the form of osteophytes, or in dense 
masses beneath and in the periosteum, occurs as a result of the same 
process by which bone tissue is normally formed. Certain rather large 
cells, called osteoblasts, which are formed along the blood-vessels, possess 
the power of depositing osseous basement substance about themselves, 
and so forming bone. Pathological new formation of bone differs from 
the normal mainly in the conditions under which it occurs. The blood- 
vessels around which the pathological bone develops, which grow out 
of the old vessels, as in the formation of granulation tissue, are irreg- 
ularly arranged and subject to a variety of abnormal nutritive and me- 
chanical conditions, so that the new bone is not usually formed in a 
series of definite systems of lamellae, but, as above described, in a series 
of irregular spiculae or masses. Moreover, as w T ill be seen further on, 
the conditions under which it is formed being liable to change, and itself 
serving no definite purpose in the economy, as does normal bone, patho- 
logical new bone is often an evanescent structure. The details of its 
disappearance will be considered below. 

5. Syphilitic Periostitis. — Syphilitic poisoning may give rise to 
simple, purulent, fibrous, and ossifying periostitis. Or, in addition to 
these, gummy tumors may be developed in the periosteum. The bone 
tissue is usually more or less involved. The gummata may be absorbed 



486 THE BONES. 

or undergo cheesy degeneration, or be converted into fibrous tissue, or 
they may suppurate. 

6. Tubercular Periostitis. — In badly nourished persons, particularly^ 
in children suffering from the so-called scrofulous diathesis (seepage 
306), a chronic purulent periostitis is frequently associated with the for- 
mation of miliary tubercles. Abscesses are apt to form in and about 
the periosteum, and when these are evacuated granulation tissue may 
develop, in which miliary tubercles are formed. In these tubercles the 
Bacillus tuberculosis maybe found. The bone is apt to be involved to a 
greater or less extent in the form of inflammatory changes or caries. 

Osteitis. 

Inflammation in bone tissue is dependent upon the same general con- 
ditions and presents essentially the same series of phenomena as inflam- 
mation in other kinds of connective tissue. But it is variously modified 
in detail by the peculiar dense and unyielding character of the base- 
ment substance, and by certain peculiarities of the blood-supply and the 
nutritive conditions under which the cells are placed. In simple exuda- 
tive inflammation, the same series of phenomena occur in connection with 
the blood-vessels, resulting in the production of serum, fibrin, and pus, 
as in other tissues; but the extent to which these changes can occur is 
limited, and constantly associated with striking alterations in the base- 
ment substance. It is these secondary alterations in the basement sub- 
stance which lend to inflammations of the bone their most peculiar 
characters, and in the prominence which these assume the fundamental 
alterations are often overlooked. The most common of these secondary 
alterations are the absorption of the hard basement substance of the bone 
and its replacement by, or conversion into, young cellular forms of fibrillar 
connective tissue or marrow tissue, and the new formation, in more or 
less atypical manner, of new bone. As a result of these changes, the 
bones in simple inflammation undergo alterations either in the direction 
of greater vascularity and increase of the spaces filled with granulation 
or marrow tissue, and so become more porous and less compact at the 
expense of the dense basement substance; or they undergo alterations 
in the direction of an increase in density at the expense of new-formed 
or pre-existing marrow spaces. Or, as is frequently the case, both series 
of changes occur either simultaneously in different regions, or follow 
one another, or are variously associated together. Very frequently one 
or the other of the opposing forms of alteration predominate, or one may 
occur to the exclusion of the other, and we thus have two prominent 
forms of inflammation, which are called rarefying osteitis or osteo-porosis, 
and condensing osteitis or osteo- sclerosis. The exact nature of the condi- 
tions under which in one case the bones become more, in another less 
dense, we do not understand. 



THE BONES. 



487 



In addition to these phases of inflammation in bone, and in frequent 
and varied association with them/ there are alterations leading to death 
and destruction of bone tissue in greater or less amount, which we call 
caries and necrosis, and also inflammatory changes, more or less charac- 
teristic, due to the influence of peculiar specific agencies, such as the 
syphilitic and tuberculous infection, and we thus recognize tubercular 
and syphilitic osteitis. Again, the production of pus is so prominent a 
feature in some cases as to represent a purulent phase of the inflamma- 
tory process. Finally, any of these forms, and commonly several of them 
at once, are variously associated with more or less marked inflammatory 
or degenerative alterations of the periosteum on the one hand, or the 
marrow tissue on the other, or of both combined. 

Rarefying Osteitis consists essentially in the formation in the marrow 




Fig. 290.— Rarefying Osteitis in Ulna of Child. 
a, isolated bone fragment with rough edges: b, marrow tissue; c, Howship's lacunae with 
osteoclasts. 



spaces, Haversian canals, or beneath the periosteum, of new, very cellu- 
lar and vascular tissue, resembling granulation or young marrow tissue, 
in connection with which, or under whose influence, the basement sub- 
stance of the bone is absorbed. The absorption of the bone occurs chiefly 
in the same way in which the bone is absorbed in normal growth, namely, 
under the influence of certain large cells, called osteoclasts, which are 
grouped around the blood vessels. If we examine a thin section of bone 
which is undergoing absorption (Fig. 200), we find the edges of the bone 
which border on the vascular surfaces irregularly indented by deep or 
shallow depressions, sometimes simple, sometimes quite complex. These 
are called Hoivship's lacunm and are usually filled or lined by larger and 
smaller granular, frequently multinuclear cells — the so-called osteoclasts^ 



488 THE BONES. 

In the larger lacunae there may be granulation tissue with loops of 
blood-vessels, with or without cells which have the morphological char- 
acters of osteoclasts. Under the influence of these peculiar cells, or of 
the new vascular tissue, the bone is gradually absorbed. In other cases 
we find irregular branching channels through the bone across the lamel- 
lae, which appear to be due to the enlargement and coalescence of the 
lacunae and canaliculi, without the direct influence of blood-vessels or 
other cells than the fixed cells of the bone. The tissue which replaces 
the absorbed bone may be very rich in small spheroidal cells, or it may 
be more or less fibrillar. As a result of this process, irregular islets of 
bone tissue may be entirely separated from adjacent bone and surrounded 
by a more or less fibrillar vascular tissue; this is most apt to occur in the 
cancellous tissue. Or the originally compact bone may become traversed 
by a series of larger and smaller irregular branching, communicating 
channels with ragged walls. These progressive alterations may cease 
and be succeeded by a new formation of bone along the edges of the 
channels or cavities; it may result in necrotic changes; the vascular 
changes may become prominent, and suppuration ensue. 

Rarefying osteitis may occur as an idiopathic disease from unknown 
causes; it is often associated with the scrofulous diathesis, with diseases 
of the joints, with fractures or other injuries to the bone; it often forms 
a predominant feature in tubercular inflammation of the bones, etc. It 
is chiefly by a rarefying osteitis that bone tissue is eroded and destroyed 
in the vicinity of tumors, aneurisms, etc., which exert pressure on the 
bones. By the same process, the sharp ends of fractured bones may be 
rounded off as healing proceeds. 

When this form of inflammation occurs in cancellous bone tissue, 
the marrow is red or gelatinous, and the bony septa may disappear alto- 
gether, so that, in extreme cases, we may have, instead of cancellous 
bone, a mass of granulation tissue. When the disease occurs in the 
articular extremity of a bone, the granulating medulla may send little 
oif shoots through the articular cartilage. These may become fused to- 
gether, and inflammation of the joint follow. The walls of the shafts 
of the long bones may be converted into spongy tissue. If, as is some- 
times the case, an ossifying periostitis occurs at the same time, the 
bone is thickened but spongy; or sometimes there are concentric layers 
of compact bone tissue, separated by rarefied bone. 

Condensing Osteitis (Osteo-Sclerosis). — This lesion is characterized 
by the new formation of bone in the walls of the marrow cavities or 
Haversian canals. The bone is formed under the influence of the blood- 
vessels and osteoblasts, as in normal bone formation, bat with less regu- 
larity. It may result in the conversion of cancellous tissue into com- 
pact bone, in the filling-up of the medullary cavity of long bones with 
more or less dense bone tissue. The compact bone, owing to the filling 



THE BONES. 



489 



of its Haversian canals, may become very dense and ivory-like. When 
the medullary cavities of long bones are involved, the yellow marrow is 
converted into red marrow by the absorption of fat and increased vascu- 
larity. It is frequently associated with ossifying periostitis. 

It very frequently follows rarefying osteitis, and under the micro- 
scope we can then often see the Howship's lacunae resulting from the 
original absorption process filled and covered in with new bone lamellae 
(Fig. 201). It is apt to occur in connection with necrosis or some 
chronic inflammation of adjacent soft parts, but it is sometimes idio- 
pathic or occurs under unknown conditions. 

Suppurative Osteitis (Abscess of Bone). — This process occurs usu- 
ally in the ends of the long bones. It begins with a rarefying osteitis. 
The medulla undergoes actual suppuration, the bone tissue is destroyed, 




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Fig. 201.— Condensing Osteitis or Osteo-Sclerosis op Ulna of Child. 
a, fragment of old bone with roughened, sinuous edges; 6, old Howship's lacunas covered with 
more recently formed bone lamella?. 



and a circumscribed cavity is formed in the boue, filled with pus and 
lined with granulation tissue. 

Less frequently, abscesses are formed in the shaft of a long bone by 
a circumscribed suppuration of the medulla. These abscesses usually 
occur in old people. They last for many years, have little tendency to 
perforation, may gradually enlarge and be accompanied by an ossify- 
ing periostitis, so that the bone is expanded. Very rarely acute suppu- 
rative osteitis, with rapid formation of an abscess, and perforation, has 
been observed. 

In some cases, instead of abscess, there may be a diffuse infiltration 
with pus of the Haversian canals or the spaces formed by rarefying 
osteitis. 

39 



490 



THE BONES. 



Tubercular Osteitis is essentially a rarefying osteitis associated with 
the formation of tubercle tissue and cheesy degeneration. The tuber- 
cles are sometimes small, scattered, and miliary in form (see Fig. 202); 
sometimes they unite to form larger and smaller masses. There may 
be extensive involvement of the medulla. There may be much simple 
granulation tissue or the formation of abscess associated with the pro- 
cess. Condensing osteitis and necrosis are not infrequently present. 
Tubercular osteitis is often associated with tubercular inflammation of 
the joints. It is most apt to occur in cancellous bone tissue, and is 
most common in the bodies of the vertebras and in the carpal and tarsal 
bones. Tubercle bacilli may be found in the tubercular masses, some- 
times in considerable numbers. 




Fig. 202.— Tubercular Osteitis. 
A miliary tubercle formed in the cancellous tissue near the joint in tubercular arthritis. 



Syphilitic Osteitis. — The syphilitic poison may induce one of the 
above-mentioned varieties of osteitis, or it may produce gummy tumors. 
The gummatous osteitis usually commences in the periosteum, which 
becomes thickened and infiltrated with cells, so that there may be a cir- 
cumscribed thickening of the periosteum, with or without distinct gum- 
mata. The vessels which extend from the periosteum into the bone 
become surrounded by new cellular tissue, which causes an enlargement 
of the canals. At this stage, if we strip off the periosteum, we drag with 
it the vessels surrounded by the new cell growth, leaving the bones be- 
neath with numerous small perforations extending inward. As the dis- 
ease progresses, the gummatous tissue around the vessels continues to 
increase, and the channels in the bone enlarge by a rarefying osteitis, 



THE BONES. 491 

and coalesce, forming large, irregular defects filled with gummatous tis- 
sue. In these masses of new tissue cheesy degeneration and the forma- 
tion of fibrous tissue occur, giving them the characteristic appearance. 
In the vicinity of these gumma-filled spaces a condensing osteitis may 
occur, both in the substance of the bone and on the surface in the form 
of osteophytes, so that the opening in the bone may be surrounded by an 
elevated, irregular ring of bone tissue. All this may occur beneath the 
uninvolved skin, or the skin may participate by a suppurative inflamma- 
tion, resulting in ulceration. These processes may be circumscribed or 
involve a large part of a bone. It is not infrequently associated with 
necrosis of larger and smaller portions of bone. The gummatous tissue 
may be absorbed and its place be more or less filled with fibrous tissue. 
Syphilitic osteitis is most frequent in the cranial bones, but may occur 
elsewhere, as in the sternum, clavicle, tibia and fibula, the ribs, etc. 

Congenital Syphilis. — The bones of young children in this condition 
may occasionally show increased density or evidences of periostitis, or 
irregular thickenings, particularly of the skull. The researches of Weg- 
ner, 1 whbh have been frequently confirmed by other observers, have 
shown that exceedingly characteristic changes very uniformly occur in 
the long bones in still-born or young children who are the victims of 
hereditary syphilis. These changes are found for the most part along 
the border zone between the epiphysis and diaphysis. It will be remem- 
bered that, in normal ossification of the long bones, the border line be- 
tween the calcification and ossification zones is narrow, sharply defined, 
and straight, or gently and evenly curved. In the syphilitic bones, on 
the contrary, this line is broader, uneven, and presents various modifica- 
tions, depending upon the stage of the disease. Wegner distinguishes 
three prominent stages, which, however, merge into one another, so that 
all intermediate forms may be seen. In the first stage there may be 
seen, between the cartilage and the new-formed spongy bone, a white or 
reddish-white zone about two mm. in breadth, with very irregular 
borders consisting of calcified cartilage, in which the linear groups of 
cartilage cells are more abundant than normal. In the second stage, 
the calcified zone, still containing an unusual number of cartilage cells, 
is broader and still more irregular and less sharply outlined against the 
ossification zone. The cartilage just beyond it is softer and almost 
gelatinous, and may contain numerous blood-vessels, islets of connective 
tissue or of calcification, or irregular ossification. In the third stage, 
the bone may be pouched out at the sides around the ossification and 
calcification zones, and the perichondrium and periosteum thickened. 
The whitish, irregular calcified zone is hard and friable. Between this 
and the new-formed bone there is an irregular, soft, gray or grayish- 

1 Virchow's Archiv, Bd. 50, 1870, p. 305. 



492 THE BONES. 

yellow zone from two to four mm. in thickness, which forms a loose, 
readily separated connection between the cartilage and the diaphysis. 
The white friable zone consists mainly of irregular rows of degenerated 
and distorted cartilage cells lying in a calcined basement substance, of 
irregular masses of atypical bone tissue, and of blood-vessels surrounded 
by variously shaped cells. The soft zone consists of more or less vascular 
tissue with homogeneous basement substance, and round and spindle- 
shaped cells. This soft zone is not sharply outlined against the adjoin- 
ing new-formed spongy bone, which, instead of consisting of the normal 
marrow spaces with bony lamellae between them, is largely composed of 
granulation tissue. 

Different stages of this faulty development may be seen in different 
bones in the same individual. According to Wegner, the lesion is usually 
most advanced in the lower end of the femur, then in the lower ends of 
the leg bones and of the forearm, then in the upper ends of the tibia, 
femur, and fibula. 

Not infrequently there is fatty degeneration of the marrow cells and 
blood-vessels, giving the marrow a reddish-yellow color. These altera- 
tions of the bones may occur, not only in children who have gummata 
in other parts of the body, but also in those in which other evidences of 
syphilitic poisoning are absent. So uniform is their occurrence that their 
presence alone suffices for the establishment of a diagnosis. 

OSTEOMYELITIS. 

In most of the inflammatory processes which affect the bones, the 
medulla has an important share, so that many conditions described as 
osteitis are really osteomyelitis. It is customary, however, to reserve 
the latter name for those cases in which the medulla is primarily or 
chiefly involved. Using the word in this sense, we may distinguish a 
so-called idiopathic and a traumatic osteomyelitis. 

Idiopathic Osteomyelitis. — At the commencement of this disease, which 
usually begins in the shaft of one of the long bones, there is hyperemia 
and oedema of the medulla, so that if the bone be opened the marrow is 
soft and of a dark-red color. A diffuse suppuration now rapidly ensues, 
and the marrow becomes streaked or mottled with gray. Occasionally, 
though not often, larger and smaller abscesses may form in the marrow. 
The inflammatory areas may be circumscribed and scattered ; or, in the 
more malignant cases, the entire marrow may become rapidly involved. 
The cancellous tissue of one or both of the epiphyses usually becomes 
involved. The disease, however, is not commonly confined to the me- 
dullary spaces. The periosteum becomes ©edematous and infiltrated with 
pus, and the surrounding soft parts may become the seat of intense in- 
flammatory changes. Abscesses of the periosteum or surrounding tissues 
are apt to form. As a result of these changes, necrosis of greater or less 



THE BONES. 493 

portions of the bone may ensue. The medullary cavity may become en- 
larged as pus accumulates, and the wall of the bone may be broken 
through, permitting the discharge of pus outward. Sometimes several 
bones may be involved at once. Secondary involvement of the joints is 
very frequent. There may be only a serous or purulent exudation ; or 
the acute and destructve inflammatory process may extend to the joint 
and produce extensive alterations. In young persons, the epiphyses very 
frequently become separated from the shaft by the destruction of the 
cartilage which binds them together. 

In the severer cases, which are often denominated, par excellence, 
malignant osteomyelitis, the changes may be very rapid and destructive. 
The mednlla becomes broken down and gangrenous ; the joints are soon 
involved; large portions of the bone, sometimes the whole shaft, necrose; 
the periosteum and surrounding parts become gangrenous ; the veins 
contain thrombi, and pyasmic infarctions and abscesses may form in 
various parts of the body. 

These lesions are, in the large majority of cases, at least due to the 
presence and action of the pyogenic cocci, the Staphylococcus pyogenes 
and the Streptococcus pyogenes, and in many of its forms may be regarded 
as one of the phases of pyaemia. 

Traumatic Osteomyelitis. — This form of inflammation may be the 
result of fracture, amputation, etc. It consists essentially in a more or 
.less diffuse suppurative inflammation of the marrow, variously associated, 
depending upon the intensity and cause of the disease, with necrosis, 
gangrene, periostitis, etc. In its more intense and destructive forms, its 
lesions are similar to those of spontaneous osteomyelitis. Similar bac- 
teria are found in the inflammatory. foci, and metastatic pygernic abscesses 
may be formed in other parts of the body. 

The distinction, then, between the so-called spontaneous or idio- 
pathic infectious osteomyelitis and traumatic infectious osteomyelitis is 
a superficial one, dependent largely upon the general manner in which 
the pathogenic bacteria gain access to the body. 1 

In the more chronic forms of osteomyelitis, there is apt to be more or 
less ossifying periostitis and osteo-sclerosis, and fistulge may form in the 
bone, through which the exudations are discharged. 

NEOKOSIS. 

By necrosis we understand the death of a larger or smaller portion of 
bone. This condition is induced by causes which deprive the bone of 
tis proper vascular supply from the periosteum and medulla. Suppura- 
tive periostitis, osteomyelitis, and osteitis, traumatic separation of the 

1 For bibliography, consult Park, "Acute Infectious Processes in Bone," Am. 
Jour. Med. Soc, July, 1889. 



494 THE BONES. 

periosteum, ulcers of neighboring soft parts, emboli, the action of phos- 
phorus vapor, and diseases, like typhus, which diminish the vitality, 
may cause necrosis. Necrosis is a pure form .of gangrene, differing from 
gangrene of soft parts in that the dead bone has at first, and may retain 
for a long time, the general outward characters of normal bone; while 
in dead soft parts the phenomena of decomposition, under the influence 
of bacteria, rapidly ensue, inducing marked complicating appearances 
in the dead tissue. 

When a portion of bone has died, an inflammation is set up at the 
dividing line between the dead and living bone. This inflammation has 
the characters of a rarefying osteitis (see above), and finally separates the 
dead from the living bone. The dead bone, or sequestrum, may remain 
smooth and unaltered, or it may be eroded by the influence of surround- 
ing pus or granulation tissue or osteoclasts. In this way, it is possible 
for the sequestrum, if it be small, to be entirely absorbed. More fre- 
quently there is a production of new bone around the sequestrum, either 
beneath the periosteum or in the substance of the bone, and this becomes 
lined with granulation tissue, from which pus may continue to be 
formed, bathing the sequestrum. 

Necrosis may involve the superficial layers, or the entire thickness of 
the wall of a long bone, or only the spongy tissue and inner layers of the 
wall, or an entire bone, or a number of different portions of the same 
bone, but it is most apt to occur in compact bone. 

The death and separation of the bone are very soon followed by the 
growth of new bone to repair the loss. The periosteum, the medulla, 
and the surrounding soft tissues may all take part in this new growth. 
The new bone is usually irregular, rough, perforated with openings, 
through which pus formed around the sequestrum may be discharged. 
If the sequestrum be removed, healing may occur by the formation of 
new bone; but the bone is usually more or less distorted by the irregular 
new ossification. 

Phosphorus Necrosis. — Under the influence of phosphorus vapor, 
periostitis and osteitis, particularly of the jaw, are apt to occur, which 
usually lead to more or less extensive necrosis, usually associated with 
prolonged and often extensive suppuration. 

CARIES. 

Caries of bone is essentially an ulcerative osteitis, resulting in pro- 
gressive molecular destruction of the bone tissue. It differs from necro- 
sis in that, in the latter, larger and smaller masses of bone die. while in 
caries the destruction is molecular and gradual. It may occur in con- 
nection with any form of osteitis, with periostitis and osteomyelitis, or 
it may be secondary to inflammatory or destructive processes in the 
joints or adjacent soft parts. The depressed surfaces of bones in which 



THE BONES. 495 

caries is progressing are rough and more or less finely jagged, and may 
be covered with granulations. The minute changes by which ulceration 
and destruction of the bone are produced in caries are somewhat analo- 
gous with those in rarefying osteitis, but there are marked degenerative 
changes in the bone cells, which may become fatty or converted into a 
granular material. Moreover, the basement substance of the bone, in- 
stead of being absorbed, may disintegrate, with the formation of larger 
and smaller masses of detritus. Sometimes the lime salts are removed 
from the basement substance, which is converted into atypical fibrillar 
tissue and fatty and granular detritus. Very extensive suppurations and 
necrosis may be associated with caries. 

Long-continued caries, especially in badly nourished individuals, is 
apt to become complicated with tubercular inflammation. 

There is very little tendency to spontaneous healing in caries, but it 
may occur, and the defects produced may be more or less supplied by 
means of new-formed bone. 

RACHITIS (EICKETS). 

Rickets is a disease affecting the development of bone, preventing its 
proper ossification. The disease usually occurs during the first two 
years of life, but may be congenital, or may occur as late as the twelfth 
year. 

The physiological growth of bones depends upon three conditions. 
They grow in length by the production of bone in the cartilage between 
the epiphysis and diaphysis; in thickness, by the growth of bone from 
the inner layers of the periosteum. At the same time the medullary 
canal is enlarged, in proportion to the growth of the bone, by the disap- 
pearance of the inner layers of bone. 

In rickets, these three conditions are abnormally affected. The car- 
tilaginous and subperiosteal cell growth, which precedes ossification, goes 
on with increased rapidity and exuberance, and in an irregular manner, 
both between the epiphyses and diaphyses, and beneath the periosteum, 
while the actual ossification is imperfect, irregular, or wanting. At the 
same time the dilatation of %the medullary cavity goes on irregularly 
and often to an excessive degree. 

If we examine microscopically the region between the epiphysis and 
diaphysis (Fig. 203), we find that the cartilage cells are not regularly ar- 
ranged in rows along a definite zone in advance of the line of ossification, 
as in normal development, but that there is an irregular heaping-up of car- 
tilage cells, sometimes in rows, sometimes not, over an ill-defined and 
irregular area. The zone of calcification also, instead of being narrow, 
regular, and sharply defined, is quite lacking in uniformity. Areas of 
calcification maybe isolated in the region of proliferating cartilage cells, 
or calcification maybe altogether absent over considerable areas. 



496 



THE BONES. 



Corresponding to these irregularities, the ossification zone is also 
irregular. New formed bone and marrow cavities containing blood- 
vessels may lie in the midst of the cartilage, or masses of cartilage may 
lie deep in the region which should be completely ossified. In other 
places, it seems as if the cartilage tissue were directly converted into an 
ill-formed bone tissue by metaplasia or direct transformation. It will 
readily be seen from this that the medullary spaces of the new-formed 
bone are irregular, and this abnormality is enhanced by the premature 
intramedullary absorption of the bone. 

The same sort of irregularity in the bone formation may be seen be- 
neath the periosteum. An excessive proliferation of cells in the inner 
layers of the periosteum, the irregular calcification which occurs about 




5i **>!** 




Fig. 203.— E^chitic Bonf. 
Showing ossification zone in a longitudinal section of a rib. 

.them, and the absence of uniformity in the elaboration of ill-structured 
bone, conspire to produce an irregular, spongy bone tissue instead of the 
compact, lamellated tissue which is so necessary here for the solidity of 
the structure. The increased cell growth between the epiphyses and 
diaphyses produces the peculiar knobby swellings which are characteris- 
tic of rickets. At the same time the medullary cavity increases rapidly 
in size, and the inner layers of the bone become spongy. The medulla 
may be congested, and fat, if it has formed, may be absorbed, and a 
modified form of osteitis may ensue. 

The result of these processes is that the bones do not possess solidity 
and cannot resist the traction of the muscles or outside pressure. The 
epiphyses may be displaced or bent, especially in the ribs, less frequently 
in the long bones. The long bones and the pelvic bones may be bent 



THE BONES. 497 

into a variety of forms. Incomplete fractures are not infrequent. Com- 
plete fractures do not usually occur until the later stages of the disease, 
when the bones have become more solid. In the head, the cranium may 
be unnaturally large for the size of the face; the fontanelles and sutures 
may remain open; the bones may be soft, porous, and hyperaamic, while 
at their edges there may be rough, bony projections beneath the peri- 
cranium. Sometimes, especially in the occipital bone, there are rounded 
defects in the bone, filled only with a fibrous membrane; this constitutes 
one of the forms of so-called craniotabes. 

It does not fall within the scope of this work to describe the various 
deformities which may occur as a result of this disease. The familiar 
pigeon breast; the rows of knobs along the sides of the chest from bend- 
ing and dilatation of the ribs at the point of junction of cartilage and 
bone; the knock-knee, bow-legs, spinal curvatures, etc., may all be the 
result of rachitic weakening of the bones. 

After a time, the rachitic process may stop and the bones take on a 
more normal character. The porous bone tissue becomes compact and 
even unnaturally dense; the swellings at the epiphyses disappear; many 
of the deformed bones may become of a normal shape. In severe cases, 
however, the deformities continue through life; especially is there a ces- 
sation of the growth of the bones in their long axis, so that the persons 
affected, are dwarfed. 

The disease may have an acute or a chronic character. The acute form 
begins usually during the first six months of life. The children are apt 
to suffer from vomiting, diarrhoea, profuse sweating, chronic bronchitis 
and pneumonia, general anaemia, and wasting. They either die or the 
rachitic process is gradually developed. The chronic form is seen in 
older children, and often in those apparently healthy. The chauges in 
the bones may take place without any constitutional symptoms, though 
there is often catarrhal bronchitis, pneumonia, and anaemia. 

OSTEOMALACIA. 

This lesion consists in the softening of fully formed hard bone tissue 
by the removal of its inorganic salts. It is to be clearly distinguished 
from rickets, whose lesions are due to a faulty development of bone, al- 
though in certain external characters the two diseases sometimes present 
considerable similarity. Osteomalacia usually occurs in adults, most 
frequently in females during pregnancy and after parturition; more 
rarely it occurs in males, and in females unassociated with the above con- 
ditions. Its cause is not known. 

Microscopical examination shows that the decalcification occurs first 
in the periphery of the Haversian canals and in the inner layers of the 
walls of the marrow spaces. As the salts of lime are removed, the base- 
ment substance at first remains as a finely fibrillated material, still pre- 



498 



THE BONES. 



serving the original lamellation. The bone cells may be changed in 
shape or degenerated. After a time, the decalcified tissue may disinte- 
grate and be absorbed, and its place occupied by new-formed marrow or 
granulation tissue. As the disease goes on, the marrow tissue is con- 
gested and red, the fat absorbed, and there is a great accumulation of 
small spheroidal cells; or the marrow may assume a gelatinous appear- 
ance. The decalcification and absorption of the bone from within may 
proceed so far that the bony substance in the cancellous tissue almost 
entirely disappears, and the compact bone is reduced to a thin, soft, de- 
calcified tissue. The disease is not always continuously progressive, but 
may be subject to temporary cessation. 

As a result of this softened condition of the bones, the weight of the 
body and the actions of the muscles may induce a series of deformities 
which are sometimes excessive: curvatures of the spine, complete and 
incomplete fractures of the bones, distortions of the pelvis, sternum, etc. 




Fig. 20 4. —Cells from the Marrow of Femur in Leukjemia. 
a, cells containing red blood-cells or fragments of red blood-cells; b, small spheroidal cells in a 
condition of fatty degeneration; c, cells like the last, but not fatty; d, nucleated red blood-cells. 

There is a tendency in this disease to a general involvement of the bones, 
but the changes are sometimes confined to single bones or groups of 
'bones. The cranium is rarely much affected. 



ALTERATIONS OF THE BONE MARROW IN LEUKAEMIA AND ANAEMIA. 

In certain forms of leukaemia, the marrow of the bones is very mark- 
edly altered. The change consists mainly in an accumulation in the 
marrow tissue of small spheroidal cells, often in a condition of fatty 
degeneration, which lie in the meshes of reticular connective tissue and 
in and along the walls of the blood-vessels. There may also be absorp- 
tion of the fat, and sometimes enlargement of the marrow cavity from 
absorption of the bone. The marrow cavity may also contain, inter- 
mingled with its other elements, nucleated red blood-cells, small 
spheroidal cells which contain red blood-cells (Fig. 204), and not infre- 



THE BONES. 



499 



quently considerable numbers of small octahedral crystals (called Char- 
cot's crystals). 

The degree to which this accumulation of cells occurs varies much in 
different cases, aud the gross appearances of the marrow are consequently 
very variable. In some cases, the marrow is soft and has a uniform red 
appearance, or it is variously mottled with gray and red. Occasionally 
circumscribed haemorrhages are seen. In another class of cases, in which 
the cell accumulation is more excessive, the marrow may be gray, gray- 
ish yellow, or puriform in appearance. 

These changes may occur in the central marrow cavity, as well as in 
the marrow spaces of the spongy bone. They may be present in several 
or many of the bones. They are usually accompanied by analogous 
changes in the spleen and lymph nodes. 

In certain cases of acute and chronic ancemia, particularly in the per- 
nicious and progressive varieties, the marrow,, especially of the larger 
long bones, may lose its yellow color from absorption of the fat, and be- 
come red. Microscopical examination of the marrow under these con- 
ditions shows considerable increase of small spheroidal cells, and some- 
times an abundance of developing nucleated red blood-cells and Charcot's 
crystals. 

In many of the acute infectious diseases, typhus and typhoid fever, 
ulcerative endocarditis, recurrent fever, etc., the bone marrow has been 
found hyperaemic and containing an unusual number of small spheroidal 
•cells. 

All of these lesions of the marrow, although our knowledge of them 
is still very incomplete, together with what is known of the physiological 
functions of the marrow, point to a close relationship between the mar- 
row and the spleen and lymph nodes as blood-producing organs. 1 . 

ATROPHY. 

In old age or in senile conditions, the bones may become atrophied by 
the absorption of the hard tissue; the medullary spaces are enlarged, the 
marrow tissue contains less fat and is often gelatinous in appearance. 
As the result of the lack of use. or from any cause which interferes with 
the nutrition of the bone, such as paralysis of the muscles or diseases of 
the joints, the bones may atrophy. In connection with atrophy there 
may be an ossifying periostitis, which results in making the bone look 
even larger than normal. Many of the conditions commonly called 
atrophy, such as the erosions of bones from tumors, etc., pressing upon 
them, are really due to a rarefying osteitis. 

1 The literature of the researches on the diseases of the spleen, which are important 
in this connection, may be found in part in Orth's " Lehrbuch der speciellen patholo- 
gischen Anatomic" Berlin, 1883. Erste Lieferung, p. 119 etseq. 



500 THE BONES. 

The bones, sometimes as the result of atrophy and sometimes from 
causes which we do not understand, are unusually brittle and liable to 
fracture. This disposition is sometimes hereditary. 

TUMORS. 

Tumors of the bone may involve either the periosteum, the compact 
bone, or the medulla, or, as is more frequently the case, two or more of 
these structures are involved at once. Tumors of the bone are usually 
accompanied by various secondary and sometimes very marked altera- 
tions of the bone tissue, osteo-porosis, osteo-sclerosis, ossifying periostitis, 
etc. The new growths are very apt to undergo calcification and ossifi- 
cation. 

Fibromata may grow either from the periosteum or medulla. Their 
most common seat is in the periosteum of the bones of the head and 
face. They are apt to form polypoid tumors projecting into the posterior 
nares, pharynx, mouth, and antrum of Highmore. Central fibromata, 
i.e., those growing from the medulla, are rare. They usually occur in 
the lower jaw, but have been found in the ends of the long bones, the 
phalanges of the fingers, and the vertebras. The fibromata may calcify 
or ossify, contain cysts, and not infrequently occur in combination with 
sarcoma. 

Myxomata are of occasional occurrence in bone. 

Osteomata. — New formations of bone, as a result of inflammatory 
processes, are, as we have already seen, of frequent occurrence in bone, 
and although not, strictly speaking, tumors, some of their forms are very 
closely allied to them, and they may therefore be conveniently men- 
tioned here. New growths of bone which arise from the surfaces are 
called exostoses or enosto*es, according to their origin from the external 
surface or interior of the bone. They may contain all the constituents 
of normal bone: bone, medulla, vessels, periosteum, and cartilage. The 
new bone may be compact and like ivory, or spongy, or contain large 
cavities filled with marrow. 

The shape of exostoses varies greatly; they may be in the form of 
sharp, narrow spiculae and processes, and, occurring in connection with 
periostitis, are called osteophytes. They may be polypoid in shape or 
form rounded tumors with a broad base. They may form a general 
enlargement of the bone, with much roughening of the surface; this 
condition is often called hyperostosis. 

The bone beneath these new growths may be normal, or sclerosed, or 
rarefied, or the medullary cavity of the bone may communicate with 
that of the exostosis. Exostoses are usually developed from the perios- 
teum, sometimes in the insertion of tendons and ligaments. They are 
very frequently multiple, and may occur at all ages, even during ute- 
rine life. 



THE BCXNES. 501 

Enostoses are developed in the interior of bones from the medulla. 
They may increase in size, with absorption of the surrounding bone, 
until they project from the surface like exostoses. Their most frequent 
situation is in the bones of the cranium and face. 

Chondromata. — These tumors may be single or multiple, and most 
frequently grow from the interior of the bone, but sometimes from the 
periosteum. They are prone to form various combinations with other 
forms of tumors, as fibroma, myxoma, sarcoma, etc. They are fre- 
quently congenital and are most common in young people. They occur 
most frequently in the bones of the hand and foot. 

There is a form of chondroma, called osteoid chondroma, which de- 
velops beneath the periosteum, most frequently in the femur and tibia 
near the knee joint, forming a club-shaped enlargement of the bone. 
The characteristics of the tissue composing these tumors are, that it 
resembles somewhat the immature bone tissue which is seen beneath the 
periosteum in developing bone. It differs from cartilage in the irregu- 
lar shape of its cells, in the fibrillation and density of the basement sub- 
stance, and in its general vascularity. On the other hand, it has not 
the inorganic contents or appearance of true bone. It resembles con- 
siderably the callous tissue forming about fractures of the bones. It 
may, however, and most frequently does, become converted, in some 
parts of the tumor, into true bone. On the other hand, combinations 
with sarcomatous tissue are of frequent occurrence (see below). 

Sarcoma. — This form of tumor is especially common in the bones. 
It grows from the inner layers of the periosteum or from the medulla, 
so that we may distinguish a periosteal and a myelogenic sarcoma. 
Sometimes the tumor attacks the bone itself so early that it is impossi- 
ble to say whether the tumor began in the periosteum or in the me- 
dulla. There is also a variety which grows close to the outside of the 
periosteum and becomes connected with it — parosteal sarcoma. 

The periosteal sarcomata usually belong to the varieties fibro-, rnyxo-, 
chondro-, and osteo-sarcoma, more rarely to the medullary variety. 
They commence from the inner layers of the periosteum, pushing this 
membrane outward. After a time the periosteum is attacked, and the 
tumor invades the surrounding soft parts. The bone beneath may re- 
main normal, or may be eroded, and gradually disappear until the tumor 
is continuous with the medulla. Portions of the tumor may be calci- 
fied, or a growth of new bone may accompany its growth. The new 
bone usually takes the form of plates, or spiculaa, radiating outward. 
The minute anatomy of these tumors is very variable. The simplest — 
the fibro-sarcomata — are composed of fusiform, round, stellate, and 
sometimes giant cells (myeloplaxes), in varying proportions, packed 
closely in a fibrous stroma. In the medullary form, the stroma is 
diminished to a minimum and the round cells are most numerous. In 



502 THE BONES. 

the chondro- and myxosarcoma, the basement substance may be hyaline 
or mucous, and the cells follow the type of cartilage and mucous tissue 
more or less closely. There is a mixed form of tumor, called osteoid 
sarcoma, which is very apt to spread and to form metastases. The 
growth consists in part of tissue corresponding to fibro-sarcoma and 
round-celled sarcoma. In addition to this, there occurs, in greater or 
less quantity, immature bone tissue, called osteoid tissue, which may in 
part become calcified, the calcification usually occurring in the central 
portions, leaving a softer peripheral zone. This form of tumor is most 
apt to occur at the ends of the long bones, and may form tumors of 
large size. It is often called, on account of its tendency to spread and 
to form metastases, malignant osteoma or osteoid cancer. 

Myelogenic sarcomata commence in the medulla and may grow rap- 
idly. The bone surrounding them is destroyed, and they project as 
rounded tumors. Most frequently new bone is formed beneath the peri- 
osteum, so that the tumor is inclosed in a thin, bony shell; sometimes 
there are also plates of bone in the tumor; sometimes the periosteum is 
unaltered; sometimes it is perforated, and the tumor invades the sur- 
rounding soft parts. The tumors are frequently very soft, vascular, and 
hemorrhagic in parts, or may inclose cysts filled with tumor detritus and 
blood. They are usually of the spindle or round-celled variety, and not 
infrequently contain giant cells. 

The parosteal sarcomata resemble the periosteal, but they appear to 
grow from the outer layers of the periosteum. They may be as firmly 
connected with the bone as the periosteal form. The periosteum may 
remain intact between the tumor and the bone, or it may disappear and 
leave them in apposition. 

Angiomata and Aneurism of Bone. — A very large number of the 
tumors which have been described under these names are really sar- 
comata, or other tumors which happened to be very vascular. Some 
authors, indeed, are disposed to deny altogether the existence of real 
•vascular tumors in bones. There are, however, reliable cases of cavern- 
ous angiomata growing between the periosteum and bone, and intimately 
connected with the latter. Whether myelogenic angiomata occur is 
doubtful. There are several cases described of cavities filled with blood 
in the interior of bones, which it is difficult to interpret. They have 
mostly been found in the head of the tibia. They are said to have con- 
sisted of single sacs composed of thickened periosteum, lined with plates, 
of bone, and filled with fluid and clotted blood. ^No large vessels com- 
municated with the sacs, but their walls were covered with a rich vas- 
cular plexus, branches of which opened into the cavity of the sac. 

Garcinomata. — Primary carcinomata are of very doubtful occurrence 
in the bones. Most of the structures thus named have doubtless been 
sarcomata. Secondary carcinomata, on the other hand, as a result of 



THE BONES. 503 

metastases or local extension, are of not infrequent occurrence and pre- 
sent various structural forms. Metastatic carcinomata may occur in the 
bones of various parts of the body at the same time, and are most apt to 
be secondary to carcinoma of the mamma. 

Cysts. — These most frequently occur in the maxillary bones, doubt- 
less in connection with the teeth. They may be unilocular or multilocu- 
lar, and contain clear serum or a mucous or brown fluid, and sometimes 
cholestearin. They may be lined with epithelium. They begin in the 
interior of the bone, and, as they increase in size, expand it until they 
may be covered with only a thin shell of bone. They may reach a large 
size, even as large as a child's head. ■ 

Dermoid Cysts are occasionally found in connection with the bones, 
particularly of the skull. 

PARASITES. 

Echinococcus and cysticercus are of rather rare occurrence in the 
bones; the former is most frequently found. 



DISEASES OF THE JOINTS. 



For a description of the dislocations, misplacements, and injuries of 
the joints, we refer to works on surgery. 

INFLAMMATION. 

Acute Arthritis. — The earlier stages of acute inflammation of the 
synovial membranes are better known. from experiments on animals than 
from post-mortem examinations. The first changes are swelling and 
congestion of the membrane, with increased growth and desquamation of 
epithelium, and infiltration of the membrane with lymphoid cells. These 
conditions are soon followed by an exudation. The exudation may be 
a clear serum, in which epithelial cells, lymphoid cells, and sometimes 
blood will be found. Or flocculi of fibrin may float in the serum, or the 
fibrin may be in excess and the serum nearly absent. Or there is an ex- 
cessive production of lymphoid cells, and the synovial sac is filled with 
pus. 

In Serous Arthritis, the accumulation of serum within the synovial 
sac is the most prominent lesion. The disease may terminate in recov- 
ery, or become chronic, or pass into the suppurative form. It may be 
caused by contusions, penetrating wounds, gonorrhoea, rheumatism, or 
it may occur without evident cause. 

Sero-fibrinous Arthritis may occur under the same conditions as those 
which lead to simple serous inflammation. The fibrin may be present 
largely as flocculi in the serum, or it may form false membranes over 
the surfaces of the joint. 

Purulent Arthritis may follow or be associated with the above forms 
of inflammation. The synovial membrane is thickened and cloudy, and 
there may be but a moderate amount of pus in the joint, and a slight 
degree of infiltration of the synovial membrane with pus cells. Under 
these conditions resolution may readily occur. 

In other cases, the accumulation of pus in the cavity may be great, 
the synovial membrane and its surrounding tissue densely infiltrated with 
pus cells. Under these conditions, granulation tissue is apt to be' found 
and the cartilages of the joints are apt to become involved. There are 






DISEASES OF THE JOINTS. 



5()5 



swelling and proliferation or degeneration of the cartilage cells; the 
basement substance becomes disintegrated, ulcerates, and exposes the 
bone, in which osteitis, caries, rarefaction, etc., may occur. The new- 
formed granulation tissue may penetrate the cartilage, absorbing the 
basement substance, and by metaplasia the cartilage tissue may be con- 
verted into embryonal or granulation tissue. The pus may break through 
the capsule of the joint and form large abscesses in the adjacent soft 
parts. Sometimes the inflammation is not only suppurative but gangre- 
nous, and runs a rapidly fatal course. The synovial membrane, articular 
cartilages, and ends of the bone, all undergo a rapid suppuration and gan- 
grene. Pysemia and septicaemia, small-pox, measles, scarlet fever, diph- 
theria, mumps, typhus fever, glanders, the puerperal condition, exposure 
to cold, penetrating wounds, and injuries, may all give rise to purulent 
synovitis. 

Chronic Arthritis may begin as such or it may be the result of pre- 
vious acute inflammation. There is an increase of fluid in the joint. 
This fluid is thin and serous, or is thickened with flocculi of fibrin and 
epithelial and lymphoid cells, or is thick, syrupy, or even gelatinous. 
The synovial membrane is at first congested, its tufts prominent. Later 
it becomes thickened, sclerosed, and anaemic; the epithelium is de- 
stroyed, and the tufts become large and projecting. From the disten- 
tion of the capsule there may be subluxations or luxations of the joint, 
or the capsule may be ruptured. 

Chronic Rheumatic Arthritis is most common in elderly persons, 
usually affecting several joints and advancing slowly and steadily. There 
is a chronic thickening of the synovial membrane and the fibrous tissue 
adjacent to it. Fluid accumulations are not common. The articular 
cartilages are apt to degenerate or ossify, or become softened and fibril- 
lated, and they may disappear. The contracting synovial membranes 
and fibrous tissue render the joints stiff, and may cause considerable de- 
formity. Not infrequently fibrous and bony anchyloses are formed be- 
tween the ends of the bones. 

Arthritis deformans. — This name has been applied to a variety of 
chronic inflammation of the joints which, combined with degeneration 
of parts of the joint and the new formation of bone, may result in marked 
deformities of the part. 

It usually occurs in elderly persons, and is apt to involve several 
joints, most frequently the hip, knee, fingers, and feet. It may be idio- 
pathic, or due to rheumatism or to injuries, or follow an acute arthritis. 
The capsules of the affected joints are thickened and sclerosed. The 
synovial fluid is at first increased in quantity; later, diminished and 
thickened. The tufts of the synovial membrane become much enlarged 
and vascular; they may be converted into cartilage. Sometimes the cap- 
sule becomes ossified. The new bone grows from the edge of the carti- 
40 



506 DISEASES OF THE JOINTS. 

lage within the capsule, and its articular surface is covered with cartilage. 
The articular cartilages are much changed. The basement substance 
splits into tufts, while the cartilage cells are increased in number. Or 
the basement substance becomes fibrous; or it is split into lamellae 
and the cartilage cells are multiplied; or there is fatty degeneration and 
atrophy. 

As a result of these changes, larger or smaller portions of the cartilage 
are destroyed, and the bone beneath is laid bare. The exposed bone may 
become compact and of an ivory smoothness. The ends of the bones 
are much deformed. They are flattened and made broader by irregular 
new growths of bone, while at the same time they atrophy. The new 
growth of bone starts from the articular cartilages. The cartilage cells 
increase in number, and the basement substance in quantity. This 
growth is most excessive at the edge of the cartilage, so that a projecting 
rim is formed there. This projecting rim may ossify next the bone, and 
at the same time new cartilage may form on its surface, so that we may 
find large masses of bone covered with cartilage. All these changes occur 
in various combinations and sequences, so that joints in this condition 
present the greatest variety of appearances. 

Arthritis uritica (Gouty Arthritis). — This disease is characterized 
by the deposit of salts of uric acid in the cartilages, bones, and ligaments, 
and also in the cavities of joints. The deposits may be in the form of stel- 
late masses of acicular crystals in and about the cartilage cells or in the 
basement substance; or they maybe deposited in the fibrillar connective- 
tissue structures of the joint in single crystals, or in the subcutaneous 
tissue about the joint as white concretions. The deposits may occur in 
repeated attacks of the disease, and are accompanied by acute inflamma- 
tory changes. They may lead to various forms of chronic inflammation 
of the joints. 

Tubercular Arthritis (Chronic Fungous Arthritis; Strumous Arthri- 
tis). — This disease may commence in the joint itself, or be transmitted 
to it from a tubercular inflammation of the bone. It is characterized by 
the formation of granulation tissue containing tubercles, sometimes in 
great quantity, and usually associated with secondary inflammatory and 
degenerative changes of surrounding parts. According to the prominence 
of one or other of these secondary alterations, several forms of tubercular 
arthritis maybe distinguished. If there is an excessive growth of granu- 
lation tissue without much suppuration, this constitutes & fungous form. 
Sometimes there is extensive suppuration, so that the cavity of the joint, 
may be filled with pus, which may be discharged through openings in 
the skin; or there may be more or less extensive formation of abscesses, 
or infiltration of the soft parts about the joint with pus. In other cases, 
there is a predominant tendency to breaking down of the new-formed 
tubercular tissue and of the tissues of the joint — ulcerative form. The 



DISEASES OF THE JOINTS. 507 

cartilage basement substance may become split into fragments and the 
cells degenerate, and thus deep and destructive ulcers of the cartilage 
be formed. Or the granulation tissue may work its way through the 
cartilage into the bone beneath, by absorption of the basement substance 
of the cartilage, with or without proliferation of its cells. Caries and 
necrosis of the underlying bone may lead to extensive destruction. Hand- 
in-hand with these alterations subperiosteal new formation of bone may 
occur, or sclerosis of the adjacent bone tissue. There may also be a 
great increase of fibrous tissue about the joint. Tubercle bacilli may be 
found in the tubercular tissue and in the exudations. 

This disease is most common in children and young persons. The 
so-called scrofulous diathesis is said to dispose to it, but local injuries 
are frequently the predisposing factors. It is most common in the large 
joints. It may occur in connection with tubercular inflammation in 
other parts of the body, but it is frequently quite local, and may remain 
so for a very long time or permanently, since general infection from 
tubercular arthritis is comparatively infrequent. 

The disease always runs a very chronic course and may destroy the 
patient's life. If recovery takes place before the cartilages and bones 
are involved, the joint is preserved; but it may be stiffened, or even im- 
movable, from the contraction of the new fibrous tissue around it. If 
the cartilages and bones are diseased, the joint is destroyed, and either 
bony or fibrous anchylosis results. Sometimes from the change in the 
articulating surfaces, and the contraction of the muscles and the new 
fibrous tissue, partial or complete dislocations are produced. 

Occasionally miliary tubercles occur in the synovial membranes in 
cases of general miliary tuberculosis, with but little accompanying simple 
inflammatory change. 

TUMORS. 

Secondary tumors of the joints as a result of local extension from the 
adjacent parts are not uncommon, and the tumors may be of various 
kinds. Primary tumors of the joints, on the contrary, are not very 
common. 

Lipoma. — A new growth of fatty tissue may begin in the other por- 
tions of the synovial membrane, push this inward, and project into the 
joint in a mass of tufts — lipoma arborescens. 

Fibroma occurs as an hypertrophy of the little tufts and fringes of 
the synovial membrane. In this way, large polypoid and dendritic 
bodies are formed. The pedicles of these growths may atrophy and even 
disappear, so that the growths are left free in the cavities of the joints. 

Corpora aliena Articulorum (Loose Cartilages in the Joints). — This 
name is given to bodies, of various structure and origin, which are 
found free or attached by slender pedicles in the cavities of the joints. 



508 DISEASES OF THE JOINTS. 

They are most frequently found in the knee; next in order of frequency 
in the elbow, hips, ankle, shoulder, and maxillary joints. They may be 
single or in hundreds. Their size varies from that of a pin's head to 
that of the patella. They are polypoid, rounded, egg-shaped, or almond- 
shaped; their surface is smooth or faceted, or rough and mulberry-like. 
They are composed of fibrous tissue, cartilage, and bone in various pro- 
portions. 

These bodies are formed in different ways. 

1. By hypertrophy of the synovial tufts and production of cartilage 
and bone in them. 

2. More frequently by a change into cartilage of portions of the 
synovial membrane. Small, flat plates of cartilage form on the inner 
surface of the synovial membrane, and these increase in size and their 
outer layers ossify. They may remain fixed in the synovial membrane, 
or they project and become detached from it, and they then appear as 
flattened concave bodies composed of bone covered with cartilage on one 
side. 

3. The growth of cartilage and bone begins in the outer layers of 
the synovial membrane or in the periosteum near the joint. The new 
growth pushes the synovial membrane inward, and projects into the 
joint as a polypoid body covered with the inner layers of the synovial 
membrane. Later the membrane atrophies, and the growth becomes 
free in the joint. 

4. There may be cartilaginous outgrowths from the edges of the 
articular cartilage. 

5. Rarely portions of the articular cartilages may be detached by 
violence or disease; or fibrinous and other concretions may result from 
arthritis, or under conditions which we do not understand. 






MUSCLE. 



LESIONS OF VOLUNTARY STRIATED MUSCLE. 

Hemorrhage. — This may occur as a result of mechanical injury; from 
rupture of the fibres by convulsive contraction, as in tetanus; or it may 
occur when the muscle fibres are degenerated, as in typhoid fever; or in 
connection with certain general diseases, as scurvy, purpura, haemor- 
rhagic diathesis, septicaemia, etc. The blood is usually readily absorbed. 

Embolic Infarction of Muscles in connection with heart disease has 
been described in a few cases, but it is rare. 

Wounds and Rupture. — When the muscle fibres are severed by 
wounds or rupture, there is more or less degeneration of the divided 
fibres, and the wound may heal by the production of granulation tissue, 
which gradually becomes converted into cicatricial tissue, thus bindings 
the severed parts together. In some cases there is a new formation of 
muscle fibres, which penetrate the cicatrix and establish muscular con- 
nection between the parts. When the wound does not gape, so that the 
severed ends are not much separated, there may be, it would seem, a 
direct re-establishment of muscular continuity by new development of 
muscle, without the formation of much new connective tissue. 

The exact way in which muscle fibres are regenerated is yet some- 
what uncertain. In many cases, there seems to be a proliferation of the 
so-called muscle corpuscles, leading to the formation of elongated cells 
or strings of cells, which are gradually converted into striated muscle. 
In some cases, the appearances would seem to indicate that connective- 
tissue cells, and perhaps white blood-cells, may participate in the forma- 
tion of new muscle fibres, but this is not certain. 1 

INFLAMMATION. 

Suppurative Myositis. — In the early stages of this lesion we find 
the muscle hyperaemic and cedematous, and the interstitial tissue more or 
less infiltrated with small spheroidal cells, doubtless the result of emi- 

1 For literature of muscle regeneration, consult Zaborowski, Arch, fur exp. Patho- 
logie u. Pharrn., Bd. 25, Heft. 5 und 6, p. 415, 



510 MUSCLE. 

gration. If the inflammation becomes intense, there may be an exces- 
sive accumulation of pus cells, either diffusely in the interstitial tissue 
or in larger and smaller masses. Hand-in-hand with this cell accumula- 
tion occur degenerative changes in the muscle fibres. By pressure their 
nutrition is interfered with, and they undergo granular, fatty, or hya- 
line degeneration. They may completely disintegrate and gangrene 
may occur, so that larger and smaller masses of the infiltrated muscle 
tissue become soft, foul-smelling, and converted into a mass of detritus 
in which but little muscle structure can be detected, and which is inter- 
mingled with bacteria. In other cases there may be larger and smaller 
abscesses formed in the muscle, the muscle tissue itself either degene- 
rating and disintegrating and mixing with the contents of the abscess, 
or being pressed aside and undergoing atrophy and degeneration. In 
some cases when the formation of pus is moderate in amount, there 
may be restoration by formation of granulation tissue between, the 
muscle fibres. This becomes gradually dense and firm, and leads to 
more or less atrophy of the muscle fibres by pressure. 

Acute suppurative myositis may accompany wounds; it is very 
common in acute phlegmonous inflammations of the skin and subcuta- 
neous tissue, and often accompanies acute infectious diseases, such as 
pyaemia, erysipelas, etc. In many cases, colonies of micrococci are 
present in the inflammatory foci. It is not infrequently seen in the 
muscles adjacent to the inflamed mucous membranes in diphtheria. 

Acute Parenchymatous Myositis. — A few cases of this disease have 
been described, in which, without lesion of the nervous system, certain 
groups of muscles, with the occurrence of fever and pain, become 
swollen, in some cases beset with small haemorrhages, soft, mottled with 
yellowish-white patches. Microscopically the muscle fibres showed 
granular and fatty, or in some cases waxy, degeneration. The cause of 
this lesion is not known. In one case, the muscles of the legs were 
thus affected in a woman who died in the first week after delivery, with 
fever and pain in the legs, and the lesion was conjecturally of infectious 
origin. 1 

Chronic Interstitial Myositis. — In this lesion there is a new forma- 
tion of connective tissue between the muscle fibres or bundles of fibres. 
This new tissue is sometimes very cellular, resembling granulation 
tissue, and this probably represents an early stage of the disease. In 
other cases (Fig. 205), we find dense cicatricial tissue crowding the 
muscle fibres apart, inducing atrophy in them, and sometimes causing 
their complete destruction. This lesion, which is the analogue of 
chronic interstitial inflammation of the internal organs, may occur in 



1 Consult MsenloTir, Centralblatt fur Nervenheilkunde, 1, 1879 ; Marchand, Bres- 
lauer Aerztliche Zeitschrift, 21, 1880. 



MUSCLE. 



511 



muscles which are adjacent to other parts which are the seat of chronic 
inflammatory processes. It may occur in muscles which are not used. 
The new formation of connective tissue would in some cases seem to be 
■secondary to atrophy of the muscle fibres. 

Myositis ossificans. — Under conditions and for reasons which we 
do not understand, there occasionally occurs, usually in young persons, 
a new formation of bone tissue in the interstitial tissue of muscles, in 
the tendons, ligaments, fasciae, and aponeuroses. This sometimes appa- 
rently starts as outgrowths from the periosteum, sometimes not. The 
bone formations are apt to commence about the neck and back, and 
may become very widespread over the body. So far as the muscles are 




Fig. 205.— Chronic Interstitial Myositis. 
The connective tissue is dense in texture, and the muscle fibres are atrophied and partially de- 
> stroyed. 

concerned, there is usually an increase of connective tissue between the 
fibres and bundles, in which new bone is formed, usually in elongated 
and sometimes in spicula-like masses. The muscle fibres undergo 
secondarily a greater or less degree of atrophy or degeneration. There 
may be fatty infiltration between the fibres, and various deformities are 
produced by the shortening and progressive immobility of the affected 
parts. 1 



1 The literature of Myositis ossificans may be found, together with a description 
of some interesting cases, in an article by Mays in Virch. Archiv, Bd. 74, p. 145. 



512 MUSCLE. 

While the above disease is a progressive and frequently a general 
one, there may be new formation of bone in muscle as a result of pro- 
longed or repeated mechanical irritation. Thus in the adductors of the 
thigh, in persons who are constantly in the saddle, or in the deltoid 
muscle of soldiers, who strike this part with their weapons in drill, there 
may be a formation of bone. 

Gumma! a and occasionally tubercles occur in the connective tissue of 
muscle. 

DEGENERATIVE CHANGES IN THE MUSCLES. 

Simple A t r op hy.— This may occur in old age, in prolonged exhaust- 
ing diseases, or as a result of pressure from a foreign body, tumors, etc. 
The muscle fibres grow narrower, the degree of narrowing frequently 
varying considerably in different parts. They usually retain the stria- 

l I 

I ' ""'■ ■ ': i ■ ■ - - ■ ■ '. ■ / ^-~ ' ' it' - t^k-^Ke* 







^tuAA-^V- 



Fig. 206.— Progressive Muscular Atrophy (Soleus muscle, longitudinal section), 
a, atrophied muscle fibre; b, degenerated muscle fibre; c, interstitial tissue; d, clusters of pro- 
liferated muscle nuclei. 

tions, but these may be obscured by degenerative changes. The sarco- 
lemma may become thickened, and there may be a considerable increase 
in connective tissue between the muscle fibres and bundles. 

Progressive Muscular Atrophy. — This lesion consists essentially in a 
combination of simple or degenerative atrophy of the muscle fibres with 
chronic interstitial inflammation, and is sometimes associated with pro- 
liferative changes in the muscle nuclei. In the earlier stages of the dis- 
ease, the muscles may be pale and soft, but exhibit otherwise to the 
naked eye but little alteration. Gradually, however, the muscle sub- 
stance becomes replaced by connective tissue, so that in marked and ad- 
vanced cases the muscles are converted into fibrous bands or cords, whose 
cicatricial contraction may induce great deformities. 



MUSCLE. 



513 



Microscopical examination shows in the early stages of the disease a 
proliferation of cells in the interstitial tissue,, so that this may have the 
appearance of granulation or embryonal tissue; also in some cases marked 
proliferative changes in the muscle nuclei (Fig. 206), leading to the forma- 
tion of new cells which may more or less replace the contractile substance 
within the sarcolemma. The new interstitial tissue increases in quantity 
and grows denser, and may crowd the muscle fibres apart (Fig. 207). The 
walls of the blood-vessels may also become thickened. Hand-in-hand 
with these interstitial alterations the atrophy of the muscle fibres pro- 
ceeds. These may simply grow narrower, retaining their striations; or 
they may split up into longitudinal fibrillae; or transversely into discoid 







Fig. 207.— Progressive Muscular Atrophy (Soleus muscle, transverse section). 
a, increased interstitial tissue; b, nearly normal muscle fibres; c, degenerated muscle fibres; 
d, atrophied muscle fibres; e, clusters of proliferated muscle nuclei. 

masses, and in this condition disappear. In other cases, a certain 
amount of fatty or hyaline degeneration may be present. These de- 
generative and proliferative changes do not, as a rule, occur uniformly 
in the affected muscles, bat some parts are affected earlier and more 
markedly than others. The atrophied muscle may be replaced by fat. 

Progressive muscular atrophy is apt to commence in the small mus- 
cles of the extremities, in many cases in the muscles of the ball of the 
thumb. It may commence in the muscles of the shoulder, the arms, or 
the back. It may have a continuous extension or it may jump single 



514 



MUSCLE. 



muscles or groups of muscles. Death may be induced by affection of the 
muscles of respiration or deglutition. 

The causes of this lesion are in many cases unknown, and there is 
considerable lack of unanimity of opinion as to whether it is primarily a 
disease of the muscles or of the nervous system. In a considerable pro- 
portion of cases, the muscle lesion is associated with atrophy of the gan- 
glion cells in the anterior cornua of the spinal cord and the development 
of connective tissue about them. In other cases, these changes in the 
cord may apparently be absent. 

It is sometimes accompanied by atrophy of the nerves which are dis- 




Fig. 208 —Pseudo-Hypertrophy of Gastrocnemii Muscle (Fatty infiltration). 
This specimen was from the case mentioned below, accompanying multiple neuroma. 



tributed to the muscles, and atrophy of the anterior roots has been de- 
scribed. 

It is probable that there are several varieties of progressive muscular 
atrophy which our present knowledge does not enable us to clearly dis- 
tinguish. Muscular atrophy in some cases follows overstraining of 
groups of muscles, or injuries, and may occur as one of the sequelse of 
typhoid fever and diphtheria. 

Atropia Musculorum lipomatosa (Pseudo-Hypertrophy of the Mus- 
cles). — In some cases, hand-in-hand with the production of new connec- 
tive tissue in the muscles and the atrophy of the muscle fibres, or after 



MUSCLE. 



515 



these changes have made considerable progress, there occurs a develop- 
ment of fat-tissue between the fibres (Fig. 208) which may prevent any 
apparent diminution in the size of the muscles, or in some cases even 
give them a great increase in size. This condition is of most frequent 
occurrence in children, and is most apt to appear in the gastrocnemii 
muscles. In the upper extremities, the deltoid and triceps are most 
frequently involved. The lesion may be symmetrical, affecting similar 
muscles on both sides of the body, or it may be unilateral. Parts of 
muscle bellies may be affected. 

The cause of this form of atrophy is not definitely known. Various 
lesions of the spinal cord have been described as occurring with it; but, 
in many cases at least, alterations of the nervous system cannot be 
detected. The writer has described a case 1 in which this lesion was 
marked in the gastrocnemii in connection with multiple false neuro- 
mata.' 2 

Fatty Degeneration, with greater or less destruction of the muscles, 
may commence with a simple swelling and fine granulation of the fibres. 




Fig. 209 —Hyaline Degeneration (so-called Waxy Degeneration) of Abdominal Muscle in 

Typhoid Fever. 

As the process goes on, smaller and larger fat-droplets appear in the con- 
tractile substance, which loses its striations and becomes friable, and 
may be entirely destroyed, leaving within the sarcolemma a mass of 
fatty detritus, which may finally be absorbed and disappear. This alte- 
ration may occur in acute parenchymatous myositis in connection with 
various forms of atrophy, in prolonged exhausting diseases, and in phos- 
phorus poisoning. 

Hyaline Degeneration. — Under a variety of conditions the muscle 
fibres undergo a peculiar series of changes, leading to their conversion 
into a translucent, highly refractile material, somewhat resembling amy- 



1 Prudden, American Journal of Medical Sciences, July, 1880, p. 134. 

2 For bibliography of muscular atrophy, consult Friedreich, " Ueber progressive 
Muskelatrophie," etc., Berlin, 1873; also " Dictionnaire encyclopedique des Sciences 
Medicales," 2 ser. i., x.; or Eulenberg"s " Real-Encyclopadie der gesammten Heil- 
kunde," article by Pick on Muskelatrophie. 



516 MUSCLE. 

loid, but not giving its micro-chemical reactions, and apparently more 
nearly allied to the material produced in the so-called hyaline degenera- 
tion. The lesion in the muscle which we are considering is commonly 
called waxy degeneration, from the peculiar appearance which the mus- 
cles present. When the lesion is far advanced and extensive, the mus- 
cles are brittle and have a grayish-yellow, translucent appearance. 
Microscopical examination of various stages of hyaline degeneration of 
muscle shows that the contractile substance of the fibres becomes at first 
swollen and granular and gradually converted into hyaline material, 
which may present the outlines of the swollen fibres, but is more fre- 
quently broken into larger and smaller shapeless clumps (Fig. 209), which 
may disintegrate and finally be absorbed. Hand-in-hand with these 
changes there usually occurs an increase in the interfibrillar connective 
tissue, and in certain cases there may be a proliferation of the muscle 
nuclei and a new formation of variously shaped cells within the sarco- 
lemma, which leads to the regeneration of the fibres. As a result of the 
brittleness of the degenerated muscles, they are apt to rupture, and in 
this way haemorrhage may occur. 

This form of degeneration may occur in progressive muscular atrophy, 
in variola, cerebro-spinal meningitis, trichinosis, in connection with 
inflammation, injuries, freezing, etc. It is, however, most marked and 
frequent in typhoid fever. In this disease the rectus abdominis and 
the adductors of the thigh are most frequently affected. 

Experimental investigations have shown that under certain conditions 
very similar appearances maybe produced in the muscles by post-mortem 
changes. It is not unlikely that a variety of changes are at present in- 
cluded under the name waxy or hyaline degeneration of the muscles. 1 

Hypertrophy of Muscle. — True hypertrophy of muscle as a patholo- 
gical condition is rare, but it has been described in a few cases. It is 
usually confined to circumscribed groups of muscles. On microscopical 
examination, the diameter of the fibres is increased, sometimes consider- 
ably, though not uniformly. The transverse striation is unaltered, and 
the muscle nuclei are in some cases enlarged. The cause of the change 
is unknown. 

TUMOKS. 

The tumors of the muscles usually develop in the connective tissue. 
Fibroma, chondroma, lipoma, myxoma, sarcoma may occur as primary 
tumors. Carcinomafa and sarcomata may occur secondarily in the mus- 
cles as a result of local extension from adjacent parts. The muscle fibres 
are, as a rule, only secondarily affected by pressure, etc., in tumors of the 

1 Consult Zenker, " Ueber die Veranderung der willkurlichen Muskeln in Typhus 
abdominalis," Leipzig, 1864; also Weihl, "Exp. Unters. ii. d. wachsartige Degene- 
ration der quergestr. Muskeln." Virch. Arch., Bd. 61, p. 253, 1874. 



MUSCLE. 517 

muscles; but there exist observations which point to the possibility of a 
proliferation of the muscle nuclei and the new formation from them of 
cells which may take part in the growth of the tumor. 

parasites. 

The Trichina spiralis is the most common parasite in the muscles. 
Cysticercus cellulosm and Echinococcus occasionally occur. 



PART IV. 



THE LESIONS FOUND 



in 



THE GENEKAL DISEASES. 



IN 



POISONING, 



AND IN 



VIOLENT DEATHS. 



TYPHOID FEVER' 



The lesions of typhoid fever are usually well marked and constant. 
They may conveniently be divided into two classes: 

I. Those which are characteristic of the disease. To this class belong 
the changes in the lymphatic nodules (follicles) of the intestines, in the 
mesenteric lymph nodes (lymph glands), and in the spleen. 

IT. Those which are very frequently found with this fever and yet 
are not peculiar to it. To this class belong the changes in the parotid 
and pancreas, the degenerations in the liver, kidneys, and voluntary 
muscles, thrombosis of the blood-vessels, infarctions, diseases of the 
lungs, and suppuration of the connective tissue in various places. 

I. The Intestines. — The lesions of the intestines consist in an inflam- 
matory enlargement and subsequent degeneration of the solitary lymph 
nodules and Peyer's patches. 

The process appears to begin with a catarrhal inflammation of the 
mucous membrane, accompanied or immediately followed by changes in 
the lymphatic follicles. The lesions in the lymphatic follicles begin 
early; they have been observed in persons who have died forty-seven 
hours after the commencement of the disease. 

The increase in size of the agminated and solitary follicles may be 
rapid or gradual. The follicles may be only slightly enlarged, or may 
project so as to fill up the cavity of the intestine. The enlargement is 
usually more marked in the agminated than in the solitary follicles. 
Usually the whole of an agminated follicle will be enlarged, but some- 
times only a part of it. If the enlargement is gradual, the different 
follicles which make up a Peyer's patch are enlarged, while the septa 
between them remain but little changed, and give the patch an uneven 
appearance. 

The patches which are only moderately enlarged are of reddish or 
reddish-gray color, are soft and spongy, and their edges blend gradually 
with the adjoining mucous membrane. The patches which are more 
intensely affected are of gray or brownish color, of firm consistence, and 

1 The most complete description of the lesions of typhoid fever is that given by 
Hoffmann, "Abdominal Typhus," 1869. 
41 



522 TYPHOID FEVEE. 

rise abruptly from the surrounding mucous membrane, or even over- 
hang it like a mushroom. The largest patches are sometimes more than 
three-eighths of an inch thick. 

The enlargement and infiltration may spread from the patches to the 
surrounding mucous membrane, so that the patches appear very large; 
a number of them may become fused together, and there may be even an 
annular infiltration entirely around the lower end of the ileum. 

The infiltration of the agminated follicles may also extend outward 
into the muscular coat, and even appear beneath and in the peritoneal 
coat as small, gray, rounded nodules. This condition is usually found 
only with a few patches in the lower end of the ileum; sometimes in the 
caecum and appendix vermiformis. These little gray nodules usually 
correspond to diseased patches beneath them; sometimes they appear to 
excite an inflammation of the peritoneum, accompanied by the produc- 
tion of numbers of similar nodules all over that membrane. Hoffmann 
describes a case in which the inflammation extended to the pleura, with 
the production of similar nodules there. 

The solitary follicles are affected in the same way as Peyer's patches. 
They may be hardly enlarged at all, or be quite prominent, or may be 
affected over a larger portion of the intestine than are the patches. 
Very rarely the solitary follicles are enlarged, while the patches are not 
at all or but slightly affected. 

The inflammation and enlargement of the agminated and solitary 
follicles are followed by a healing process. The character of this process 
varies according to the intensity of the previous inflammation. 

1. If the disease was mild and the enlargement of the follicles mod- 
erate, the enlargement gradually disappears and the follicles resume 
their normal appearance. 

2. In moderate enlargements, the retrograde processes affect first the 
follicles, and leave the septa between them still swollen and prominent. 
This gives to the surface of a patch a reticulated appearance. After a 
time, however, the entire patch becomes flattened and uniform. 

3. The solitary follicles or the separate follicles of a patch soften, 
break down, and their contents are discharged with some attendant 
haemorrhage. This leaves a bluish-gray pigmentation in the situation of 
each follicle. This pigmentation may remain for years. 

4. In more severe types of the disease, the enlargement of the folli- 
cles ends in ulceration. This takes place in two ways : 

(a) The enlarged follicles soften, break down, and discharge into the 
intestine. In this way are formed small ulcers. These ulcers increase 
in size by the same softening process, which gradually attacks their edges, 
and in this way ulcers of large size may be formed. The ulcers may ex- 
tend outward only to the peritoneal coat, or they may involve the peri- 
toneal coat also and perforate. 






TYPHOID FEVER. 



523 



(b) In the severest forms of the disease, considerable portions of the 
enlarged patches slough, are detached, and leave large ulcers with thick, 
overhanging edges. The slough may involve only the follicles, or it may 
involve also the muscular and peritoneal coats. These ulcers also may 
afterward increase in size, and several of them may be joined to- 
gether. 

If the patient recovers, the ulcers cicatrize, their edges become flat- 
tened, their floors are converted into connective tissue covered with cy- 
lindrical epithelium. 

Both forms of ulceration sometimes end in perforation. This is ef- 
fected by the extension of the ulcerative process through the peritoneal 
coat or by the rupture of the floor of the ulcer. Peritonitis and death 
are the usual result. In rare cases, however, the patient recovers and 
the perforation is closed by adhesions. 

The minute changes which take place in the course of the intestinal 
lesion are as follows : 

At first the blood-vessels around the follicles are dilated and con- 
gested, while the follicles are swollen and the epithelium falls off. Then 
the follicles increase largely in size from a growth of new cells. The 
new cells are, in part, similar to the lymphoid cells which normally 
compose the follicles; in part are large, rounded cells, some of which con- 
tain several nuclei. The production of new cells is not confined to the 
follicles, but extends also to the adjacent mucous membrane. In many 
cases also, little foci of the same cells are found in the muscular, subse- 
rous, and serous coats. This increased number of cells compresses the 
blood-vessels, and the parts become anaemic. Soon the cells degenerate, 
either by granular degeneration of individual cells or by gangrene of part 
of a follicle. In either case the degenerated portion is eliminated into the 
intestine, and leaves an ulcer of which the floor and edges are infiltrated 
with cells. After this the cell growth goes on, and the ulcer enlarges, 
or the cells are gradually replaced by connective tissue, and cicatrization 
follows. 

The lesions we have described are found most frequently and most 
developed in the lower part of the ileum. They are not always, however, 
confined to this situation. Enlarged and ulcerated follicles may be found 
over the entire length of the ileum, and even in the jejunum. They may 
also extend downward and be found in the colon, even as far down as 
the rectum. The same changes may also take place in the appendix 
vermiformis. 

Besides the regular typhoid lesions of the intestines which have been 
described, we occasionally meet with others of a more accidental charac- 
ter. 

Gangrene of the intestinal wall sometimes occurs. It most frequently 
involves a portion of the wall corresponding to an ulcer, but may also 



524 TYPHOID FEVER. 

affect other portions where no ulcer exists. The process may terminate 
in perforation or in healing. 

Croupous Inflammation may attack the mucous membrane of either 
the large or small intestine. The mucous membrane between the 
typhoid ulcers is covered and infiltrated with an exudation of fibrin and 
pus. 

Peritonitis of a mild type is a frequent accompaniment of the intes- 
tinal lesions. It appears to have but little influence on the course of the 
disease. 

Severe peritonitis is usually due to perforation, less frequently to 
ulcers which reach the serous coat but do not perforate. When there is 
infiltration of the serous coat with the typhoid new growth, the perito- 
nitis may be accompanied by a production of little gray nodules of the 
same character throughout the peritoneum. 

Infarctions of the spleen, inflammation of the ovaries, and perfora- 
tion of the gall bladder are sometimes the cause of peritonitis. 

Haemorrhage from the intestines is merely due to the inflammatory 
swelling and congestion of the mucous membrane, and is slight; or it is 
due to the ulceration of the follicles and destruction of the blood-vessels, 
and is then often profuse. 

Mesenteric Lymph Nodes. — The mesenteric nodes undergo the same 
changes as the follicles of the intestines, and are usually affected in a 
degree corresponding to the intensity of the intestinal lesion. 

The nodes are at first congested and succulent; then there is a pro- 
duction of lymphoid cells and large cells, as in the intestinal follicles 
(Fig. 152), and the node becomes enlarged. When the enlargement 
has reached its full size, the congestion diminishes and the cells begin 
to degenerate. The degeneration may take place slowly, and then the 
node gradually returns to its normal condition; or more rapidly, and 
then little foci of softened purulent matter are formed. If the patient 
recovers, the small foci are absorbed, leaving a fibrous cicatrix; the 
larger foci become dry, cheesy, and inclosed in a fibrous capsule. The 
inflammation of the nodes may produce a local or general peritonitis. 

The Spleen. — In nearly every case of typhoid fever, the spleen is en- 
larged. This enlargement begins soon after the commencement of the 
disease, increases rapidly until the third week, remains stationary for a 
few days, and then diminishes. The organ is congested, of dark-red color, 
and of firm consistence while it is increasing in size. After it has 
reached its maximum size, its consistence becomes soft, and there is a 
considerable deposit of brown pigment. The enlargement appears to be 
due to the congestion and to an increase of the normal elements of the 
spleen. 

In rare cases, the softened spleen is ruptured, with an extravasation 
of blood into the peritoneal cavity. 



TYPHOID FEVEE. 525 

There may be infarctions of the spleen, which sometimes soften and 
cause peritonitis. 

II. The second class of lesions comprises those which are frequently 
found with typhoid fever, but are not peculiar to it. 

The Mouth. — A number of changes are found about this region. The 
follicles at the root of the tongue and the tonsils may be enlarged; the 
muscles of the tongue may undergo waxy and granular degeneration; 
gangrenous ulcers may attack the floor and sides of the mouth and 
destroy large areas of tissue. 

The Pharynx may be the seat of catarrhal or croupous inflammation, 
producing superficial and deep ulcers. 

The Parotid is, in a moderate number of cases, the seat of an inflam- 
mation which tends to suppuration. In this process, both the glandular 
acini and the connective tissue between them are involved. Which of 
the two has the larger share in the process is still in dispute. 

A slight enlargement and induration of the parotid and submaxillary 
glands is said by Hoffmann to be a frequent lesion, and to depend on in- 
crease of the gland cells and dilatation of the follicles with their secretion. 

The Pancreas undergoes changes similar to those in the salivary 
glands. It becomes at first swollen and red, then hard and grayish, 
then yellow. The vessels are at first congested, afterward there is in- 
crease of the gland cells, and lastly degeneration. 

The Liver may preserve its normal character or may present 
changes. 

In many cases, the organ will be found soft and flabby. Minute ex- 
amination then shows that the liver cells have undergone degeneration. 
They are filled with fine granules and small fat-globules, and the de- 
generation may go on so far that the outlines of the hepatic cells are 
lost and nothing but a mass of granules can be seen. 

Less frequently we find in the liver very small, soft grayish nodules 
resembling those found in the peritoneum. They are situated along the 
course of the small veins, and there is, at the same time, a diffuse infil- 
tration of lymphoid cells along the small veins. The nodules consist of 
lymphoid cells; they are often too small to be distinguished with the 
naked eye. 

The Heart. — In a considerable number of cases, the muscular tissue 
of the heart is altered. The heart feels soft and flabby; it is of grayish 
or brownish color; the muscular fibres are infiltrated with fine granules, 
and sometimes with brown pigment. Or the heart is firm, but friable 
and easily torn, its cut surface glistens, and its muscular fibres are in 
the condition of hyaline degeneration. 

Thrombi in the cavities of the heart and vegetations on the valves 
are sometimes found. Detached fragments of these may be lodged as 
emboli in the different arteries. 



526 TYPHOID FEVEE. 

The Arteries. 1 — There may be an acute inflammation of the arteries, 
especially at the commencement of convalescence. There are two varie- 
ties: an obliterating and a parietal arteritis. In the obliterating arteritis 
there is infiltration of all the coats of the artery, with roughening of the 
intima and the formation of a thrombus within the vessel, and this is 
followed by dry gangrene of the parts supplied by the artery. In the 
parietal variety the wall of the artery is infiltrated with cells, but the 
intima is not roughened and no thrombus is formed. 

The Veins. — Thrombosis of the larger veins, especially of the femoral 
vein in the third and fourth weeks of the disease, is not uncommon. 

The Larynx is very frequently the seat of catarrhal inflammation, 
with or without superficial erosions. Less frequently there is croupous 
inflammation, followed in some cases by destructive ulceration. 

The Lungs. — Catarrhal inflammation of the large bronchi is very 
common. Broncho-pneumonia occurs in two forms. There may be a 
severe inflammation of most of the bronchi of both lungs, with cellular 
infiltration of the walls of the bronchi and zones of peribronchitic pneu- 
monia; or there is an intense general bronchitis, with lobules of the 
lung corresponding to obstructed bronchi, either collapsed or inflamed, 
or both. 

From the long-continued recumbent position of the patients, the pos- 
terior portions of the lungs become congested, dense, and unaerated. 
Sometimes, in addition to this, irregular portions of the lungs become 
hepatized. 

Less frequently there is regular lobar pneumonia. 

There may be infarctions in the lungs. 

Gangrene of the lungs is occasionally found, either associated with 
lobular pneumonia or with infarctions, or as an independent condi- 
tion. 

The Kidneys very frequently present the lesions of parenchymatous 
nephritis. They may contain infarctions. 

The Ovaries. — Haemorrhage and gangrenous inflammation have been 
observed in rare cases. 

The Testicles. — Orchitis has been described by Ollivier. 2 It generally 
is developed during convalescence; it is unilateral; it usually affects the 
testicle alone, less frequently the epididymis; it terminates in suppura- 
tion in nearly one-fourth of the cases. 

The Brain. — Acute meningitis, thrombosis of the venous sinuses, 
and obliterating endarteritis of the cerebral arteries occasionally are ob- 
served. 

1 Barie, Rev. de Med., Jan., Feb., 1884. Keen, " Toner Lectures on the Surgical 
Complications of the Continued Fevers/ 5 1877. 

2 Rev. de Med., Nov. and Dec, 1883. 



TYPHOID FEVER. 527 



I 



The Voluntary Muscles, especially the abdominal muscles, the ad- 
ductors of the thigh, the pectoral muscles, the muscles of the diaphragm 
and of the tongue, frequently undergo the hyaline degenerative changes 
described under muscle lesions (Fig. 209). 

The Shin. — Gangrenous inflammation of the skin frequently occurs 
in the form of bed sores, affecting especially the skin over the sacrum 
and trochanters, where it is subjected to the constant pressure of the 
bed. 

There may be suppurative inflammation of the connective tissue in 
any part of the body. Perhaps the most important of these local sup- 
purations is that which produces retro-pharyngeal abscesses. 

The Bacillus of Typhoid Fever. — The presence of a bacillus in vari- 
ous parts of the body in typhoid fever, in a considerable proportion of 
the cases examined, has been well established by a large number of ob- 



i&^(. 




Fig. 210.— Cluster of Typhoid Bacilli in the Spleen. 

servers. This bacillus does not occur in the body, so far as is known, 
except in connection with this disease. 

In the early stages of the disease, the bacillus may be found in the 
lymphatic structures of the intestines, and in the mesenteric lymph 
nodes and the spleen. It may be present in the kidney, liver, lungs, 
and in the blood, and is often found in enormous numbers in the intes- 
tinal contents. In the viscera it is apt to occur in larger and smaller 
masses or clusters (see Fig. 210). 

The typhoid bacillus is usually about three times as long as broad 
(Fig. 211), being about one-third as long as the diameter of a red blood- 
cell. It is rounded at the ends, and frequently contains rounded struc- 
tures which have been regarded as spores, but which further researches 
have led us to believe are not spores but vacuoles. 

The typhoid bacillus can be readily cultivated on the ordinary culture 
media at room temperatures. It forms delicate, bluish white, sinuous- 



528 TYPHOID FEYEK. 



• 



edged, spreading colonies on the surface of nutrient gelatin, which it does 
not fluidify. Several other bacteria grow in a similar way on gelatin, 
but the mode of growth of the typhoid bacillus on boiled potatoes is its 
most marked culture characteristic; for, unlike any other known species, 
it forms on the surface of the potato an invisible pellicle. If, however, 
the potato be made slightly alkaline, the surface growth becomes evi- 
dent. In cnltures, the typhoid bacilli often cling together end to end, 
forming long, thread-like structures (Fig. 211). The bacilli in fluids are 
actively mobile. 

Inoculations of the typhoid bacillus into animals, while not producing 
a disease in all respects like that in the human subject, may cause death 
with symptoms and lesions as closely resembling those in man as we are 
often able to produce in animal experimentation. Altogether the evi- 
dence that typhoid fever in man is produced by the typhoid bacillus, and 
by this alone, is so strong as practically to amount to a demonstration. 

It is probable that the symptoms and lesions of typhoid fever are 
largely due to the absorption of a ptomaine which is produced as the 
result of the life processes of the bacteria at the point of their greatest 
accumulation and activity, namely, in the intestinal canal. 




Fig. 211.— Typhoid Bacilli from Gelatin Culture. 

Typhoid fever appears in a large proportion of cases to be communi- 
cated by means of drinking water which has been polluted with the ex- 
cretions of persons suffering from the disease. 

The bacilli are capable of living for considerable periods in water as 
well as in ice. They have been repeatedly fonnd by biological examina- 
tions in polluted drinking water to which external evidence has pointed 
as the source of a typhoid epidemic. 

METHODS OF STAINING THE TYPHOID BACILLUS. 

The bacilli, when taken from cultures, stain readily with the ordinary 
aniline dyes, such as fuchsin and gentian violet (see page 96). 

In sections of the organs they do not take the stain so readily. They 
are decolorized by Gram's method. 

One of the most satisfactory solutions for this purpose is that of 
Ziehl, which is made as follows: 

Filtered Saturated Aqueous Solution of Carbolic Acid.. .90 
Saturated Alcoholic Solution of Fuchsin 10 

The sections are soaked for half an hour in this solution and then 






TYPHOID FEVER. 529 

decolorized by alcohol, cleared in oil of cedar, and mounted in balsam. 
The decolorization should be done carefully, the section being examined 
from time to time as it proceeds, so as to avoid the removal of too much 
color. The nuclei should remain faintly colored, but not so much so as 
to conceal the clusters of more deeply stained bacilli. 1 

1 For literature of typhoid bacillus, consult a resume by Seitz, Centralblatt fur 
Bakteriologie u. Parasitenkunde, Bd. 2, No. 23, 1887. 

42 



TYPHUS FEVER 



This disease has not, so far as we know, any characteristic lesion; 
but yet after death we may find a number of morbid conditions, such as 
are common to the infectious diseases. 

The entire body has a teudency to rapid putrefaction. 

The blood is often darker and more fluid than in other diseases. 

The voluntary muscles may undergo waxy and granular degeneration. 

The brain and its membranes may be congested. 

The mucous membrane of the pharynx and larynx may be the seat 
of catarrhal or croupous inflammation. 

In the lungs there may be bronchitis, broncho -pneumonia, or hypo- 
static congestion. 

The walls of the heart may be soft and flabby. 

The agminated glands of the ileum, and the mesenteric nodes, may 
be a little swollen. 

The spleen is often large and soft. 

The kidneys are frequently the seat of parenchymatous nephritis. 

The nature of the infective agent in typhus is unknown. 






RELAPSING FEVER. 



Synonyms. — Typhus recurrens; Famine fever; Spirillum fever. 

The Skin may be jaundiced; it may be mottled by extravasations of 
blood. 

TJie Brain and Spinal Cord are unchanged. 

The Pharynx and Larynx may be the seat of catarrhal or croupous 
inflammation. 

The Lungs. — There may be bronchitis, broncho-pneumonia, lobar 
pneumonia, hypostatic congestion, and pleurisy. 

The Heart is often soft and flabby, with degeneration of its muscular 
fibres. There may be ecchymoses in the pericardium. 

The Stomach and Small Intestine may be congested; there may be 
ecchymoses in the mucous membrane; there may be catarrhal inflamma- 
tion. 

The Colon may be the seat of catarrhal or croupous inflammation. 

The Mesenteric Nodes may be swollen. 

The Liver is often enlarged and the hepatic cells are swollen and 
granular. 

The Spleen is large and soft, like the spleen of typhoid fever. The 
change in its consistence is so marked that the spleen may rupture spon- 
taneously during life. The spleen may also contain infarctions of differ- 
ent sizes; some are red, some yellow, some necrotic. Those which are 
necrotic may give rise to a local or general peritonitis. 

The Kidneys show the lesions of parenchymatous nephritis. 

The Bones. — Degenerative changes in the medulla of the bones have 
been described by Ponfick. 1 

Bacteria. — In the blood of all parts of the body during the febrile 
attacks may be found, in very large numbers, a long, slender spirillum 
called Spirochete Obermeieri. It disappears from the blood during the 
afebrile intervals. The organism is from sixteen to four pi in length, 
and performs rapid, undulating movements (Fig. 212). The inocula- 
tion of monkeys with the blood of relapsing-fever patients which contains 

1 Virch. Arch., Bd. 60, p. 153. 



532 



RELAPSING FEVER. 



the bacteria induces a similar disease. Pure cultures have not as yet 
been made of these bacteria, but for the reasons indicated, and since the 
organism has never been found except in connection with the disease, 




Fig. 212.— Spirochete Obermeieri in the Blood in a Case of Relapsing Fever. 

there is every reason for believing that the Spirochete Obermeieri is the 
cause of relapsing fever. 



ACUTE CEREBRO-SPINAL MENINGITIS. 



This is an acute infections disease, characterized by an exudative in- 
flammation of the pia mater of the brain and spinal cord. The degree 
of the lesion in the meninges varies greatly, depending upon the period 
at which death occurs. In some cases, when death occurs early in the 
disease, there may be to the naked eye no evident change in the mem- 
branes, or a moderate serous infiltration. In these cases, the microscope 
may reveal a moderate degree of extravasation of leucocytes in the vicin- 
ity of the vessels. In the well-marked, cases, the pia mater of the brain 
and cord is more or less densely infiltrated with serum, fibrin, and pus. 
This may occur over the convexity and base of the brain, and is fre- 
quently most marked in the latter situation. In the cord, the infiltra- 
tion may occur over the anterior and posterior surfaces; but in many 
cases, probably owing to the recumbent position of the patient, it is most 
marked on the posterior surface. The ventricles of the brain and the 
central canal of the cord may contain turbid serum mingled with pus- 
cells, and sometimes blood-cells. The membranes and underlying nerve 
tissue may be hyperaemic and the seat of capillary haemorrhages. Rarely 
a small amount of pus and fibrin may be found between the pia and 
dura mater. 

In protracted cases, the ventricles may be dilated with serum, and the 
exudation in the meninges may become fatty or dense and cheesy. 

While the above are the characteristic lesions of this disease, there 
are a number of secondary changes in different parts of the body which 
are not constant, but which occur with sufficient frequency to render 
their mention necessary. There may be subserous punctate haemor- 
rhages in the endocardium; petechias in the skin; hyaline and granular 
degeneration in the voluntary striated muscle; occasional multiple ab- 
scesses in various parts of the body; suppurative inflammation of the 
joints; parenchymatous degeneration of the heart, liver, and kidneys; 
and swelling of the gastro-intestinal lymphatic apparatus. 

Oerebro-spinal meningitis may occur by itself or in connection with 
some other acute infectious disease, such as acute lobar pneumonia, my- 
cotic ulcerative endocarditis, pyaemia, multiple suppurative arthritis, 
otitis media, puerperal fever, typhoid fever, etc. 



534 ACUTE CEREBROSPINAL MENINGITIS. 

The lesions are essentially the same in epidemic and in sporadic cases 
of acute cerebro-spinal meningitis, and there is much reason to believe 
that in both modes of occurrence the disease is caused by bacteria. But 
studies of the epidemic form of the disease have not yet been made by 
the new methods, so that we can say nothing definite about its causa- 
tion. 

On the other hand, numerous careful studies have been made on the 
bacteria occurring at the seat of lesion in sporadic cases occurring both 
with and without complicating lesions in other parts of the body. 

The Streptococcus pyogenes has been demonstrated in a few cases, 
occurring in connection with suppurative inflammations elsewhere. 

The Pneumococcus of Fraenhel (see page 238) has been found in 
several cases, and in some of these without any lung lesion. Weichsel- 
baum has described the occurrence in several cases of a diplococcus not 
known to occur elsewhere, which was found largely confined to the pus 
cells, and which he called Diplococcus intracellular is meningitidis. 

Animal experiments with this as well as the pneumococcus would in- 
dicate that they stand in a causative relation to the disease. Some other 
scattering forms of bacteria have been described, but not with sufficient 
frequency and definitiveness to enable us to judge of their significance. 

It seems probable, therefore, from what we know at present, that 
several forms of bacteria are capable of causing acute cerebro-spinal 
meningitis. Which is the most frequent and important it remains for 
further researches to show. '- 

1 For literature and further details consult Weichselbaum, Fortschritte der Medicin , 
September 15th, 1887; Goldschmidt, Centralblatt fur Bakteriologie, Bd. 2, No. 22; 
Neumann and Schaefer, Virchow's Archiv, Bd. 109, p. 477. 



DIPHTHEEIA. 



Diphtheria is an acute infectious disease, usually characterized by a 
croupous inflammation on some of the mucous membranes or on the 
surface of wounds. 

The mucous membranes which are the most frequently affected in 
diphtheria are those of the tonsils, pharynx, soft palate, nares, larynx, 
and trachea; less frequently those of the mouth, gums, oesophagus, and 
stomach. 

The local inflammation may present various phases which represent 




Fig 213.— Diphtheria of the Trachea. 
Section through the pseudo-membrane and underlying tissue, showing large numbers of strep- 
tococci. 

clinical types of the disease. Thus there maybe a simple redness of the 
affected surfaces which leaves no trace after death, or a catarrhal in- 
flammation. On the other hand, in the more marked forms of the 
lesion there may be a fibrous exudate which infiltrates the mucous mem- 
brane, or, intermingled with pus cells, epithelial cells, red blood- cells, 
bacteria, and granular material, forms a thick or thin pellicle on the af- 
fected surfaces. This pellicle may undergo coagulation necrosis, and 
hand-in-hand with this there may be superficial or deep coagulation ne- 
crosis of the mucous membrane. 



536 DIPHTHERIA. 

Bacteria of various forms are commonly present in the false mem- 
brane, and some of the forms may penetrate deeply into the underlying 
tissue. 

The false membrane in diphtheria is thus formed by a combination 
of inflammation and necrosis, the extent of the necrosis and the amount 
of inflammatory products varying in the different cases. 

The pseudo-membrane may disintegrate or exfoliate, with or without 
loss of tissue in the underlying mucous membrane. Phlegmon, abscess, 
and oedema are liable to occur as local complications. Adjacent and dis- 
tant lymph nodes are apt to be swollen, and the liver, kidneys, and sali- 
vary glands to present parenchymatous degeneration. 

Catarrhal bronchitis, and broncho-pneumonia or lobular pneumonia, 
frequently complicate diphtheritic lesions of the upper air passages and 
fauces. 

Prolonged series of studies have shown that diphtheria is caused by 
bacteria, which apparently induce the croupous inflammation by their 



(0& 




Fig. 214.— Streptococcus Diphtheria. From a beef -tea culture. 

local growth, and the systemic effects by the absorption of a ptomaine 
produced by the germs at the seat of local lesion. 

It is not unlikely that more than one species of bacteria is capable of 
inducing that series of symptoms or lesions which we call diphtheria. 

Loeffler and others have isolated a slender bacillus from the pseudo- 
membrane in several cases, which they are disposed to believe to be the 
cause of the disease in the cases which they studied in Germany. 

On the other hand, bacterial studies on cases of diphtheria occurring 
in New York have failed to reveal the presence of Loeffler's bacillus, but 
have shown the very constant presence in and about the local lesion 
(Fig. 213) of a streptococcus which appears to be identical with the 
streptococcus of suppuration and of erysipelas, and which there is much 
reason for believing is the cause of the disease (Pig. 214). These bac- 
teria, which have been temporarily called Streptococcus Diphtherial, are 
not found in any considerable numbers in the viscera. 1 

1 For a resume of earlier bacterial investigations on diphtheria, and the results of 
recent studies on cases occurring in New York, see " Studies on the Etiology of Diph- 
theria" (Prudden), Am. Jour. Med. Sc, April and May, 188 9. 



ASIATIC CHOLERA. 



In some cases of cholera there are no marked changes to be found 
after death. 

If death occurs during the invasion of the disease or in the stage of 
collapse, in the more marked cases the appearances are as follows : 

The bodies remain warm for some time, and the temperature may 
rise for a short time after death. The rigor mortis begins soon and 
lasts for an unusually long time. The muscles sometimes exhibit a pe- 
culiar spasmodic twitching before the rigor mortis sets in, especially the 
muscles of the hand and arm. 

The Skin is of a dusky gray color, the lips, eyelids, fingers, and toes 
of a livid purple. The ends of the fingers are shrivelled, the cheeks and 
eyes are fallen in. 

The Brain. — The sinuses of the dura mater are filled with dark, thick 
blood. The pia mater may be normal, or oedematous, or ecchymosed, 
or infiltrated with fibrin. The brain is usually normal, but may be dry 
and firmer than usual. 

The Lungs are retracted and anaemic, the pleura may be dry or 
coated with fibrin. 

The Heart is normal. 

The Peritoneum may be dry or coated with a layer of fibrin. 

The Stomach is usually unchanged, but may be the seat of catarrhal 
inflammation. 

The Small Intestine. — There may be ecchymoses in the mucous mem- 
brane: the mucous membrane maybe soft and oedematous; there maybe 
general congestion, or the congestion'may be confined to the peripheries 
of the solitary and agminated glands, and these glands may be swollen; 
or there may be croupous inflammation and superficial necrosis. All 
these changes are regularly most marked at the lower end of the small 
intestine. There is apt to be post-mortem desquamation of the epithe- 
lium. The characteristic rice-water fluid may be found in the intestines 
after death, or instead of this a dark-colored, bloody fluid. 

The Large Intestine is usually normal, but in some epidemics croup- 
ous inflammation occurs in a considerable number of cases. 
43 



538 



ASIATIC CHOLERA. 



The Liver and Spleen undergo but few changes; they may be anaemic 
and flabby. 

The Kidneys are often increased in size, with white and thickened 
cortex and congested pyramids. The epithelium of the cortex tubes con- 
tains coarse granules and fat-globules. The tubes contain cast matter 
and broken-down epithelium. These changes may be looked upon as 
being simply of a degenerative character or as the results of a parenchy- 
matous nephritis. 

The Utertis and Ovaries may be congested and contain extravasated 
blood. 

If the patient does not die until the stage of reaction, the body does 
not present the same collapsed appearance, and there are often inflam- 
matory changes in different parts of the body, especially in the larynx, 
the lungs, the stomach, and the intestines. 




Fig, 215.— Spirillum Cholera Asiatics. From a beef-tea culture. 



According to recent researches by Koch, which have been abundantly 
confirmed by others, there are constantly present in the small intestines 
of cholera patients, during the early and active stages of the disease, char- 
acteristic curved bacilli which are not known to occur in the body under 
any other conditions, and which have been proved to cause the disease. 
These bacilli are from 0.8 to 2.0 // long, and are sometimes slightly, 
sometimes considerably curved (see Fig. 215). When growing, the indi- 
vidual bacilli are apt to cling together by their ends, forming S-shaped 
figures or spirils of considerable length. They are therefore often called 
Spirillum cholera asiaticce. From the curved shape of the individuals 
they are also often called " comma bacilli." They maybe present in 
moderate numbers in and beneath the mucous membrane of the intes- 
tine, and in very large numbers in the intestinal contents and in the 
dejections in the acute forms and early stages of the disease. 



ASIATIC CHOLERA. 539 

In the process of their growth and multiplication in the intestinal 
canal, they apparently produce a poisonous ptomaine, the local action and 
absorption of which into the body fluids produce the symptoms and lesions 
of the disease. The systemic effects appear to be in the nature of a sep- 
tic intoxication. The cholera bacillus may retain its vitality for a con- 
siderable period in water, and on moist substances, such as damp linen, 
earth, and vegetables, may increase in numbers with great rapidity. 

A temperature of from 30°-40° 0. is most favorable for their growth. 
At about 16° 0. their proliferative activities cease, but they are not 
killed by — 10° C. They are readily killed by drying, and the presence 
of acids is very inimical to their growth. 

There is not sufficient evidence that they form spores, and their period 
of life is short. 

The cholera bacillus is readily cultivated on artificial culture media, 
such as gelatin, agar, milk, beef -tea, potatoes, etc. In fluids it is capa- 
ble of performing active movements. 

While they may be readily stained by the ordinary methods when 
present in the dejecta, their morphological characters are not absolutely 
distinctive, since several forms of curved bacilli belonging to the same 
group and closely resembling them have, under varying conditions, been 
found in the dejecta and in the mouth. 

It is often of the highest importance to determine, at the earliest pos- 
sible movement, whether or not a suspected case be one of Asiatic 
cholera or some other form of acute intestinal disorder, so that the 
proper measures may be instituted to prevent the spread of the disease. 
The characters which are developed in the cultures of the cholera bacil- 
lus enable an expert biologist to distinguish this organism from all other 
known forms. 

G-elatin plate cultures are made in the usual way (see page 101) from 
the intestinal contents, very small portions being taken. A considerable 
number of plates should be made of varying dilutions and kept at about 
21° C. (70° F.). Usually after about twenty-four hours, the colonies 
of the cholera germ appear as small, rounded, grayish, granular bodies 
with rough edges. As the colonies grow, they become more coarsely 
granular, and after a time look as if composed of strongly refractile 
granules, like particles of pounded glass. The gelatin becomes fluidified 
around the growing colony, which sinks into the fluid-filled pit thus 
formed. In gelatin tubes inoculated in the usual way with the cholera 
bacillus, the gelatin is fluidified along the puncture line, but most rapidly 
at the surface, where a small air bubble usually lies at the top of the 
fluidified pit. 

On potatoes the cholera bacillus grows but slightly at ordinary tem- 
peratures, but in the thermostat, at the temperature of the body, it grows 
rapidly, forming a light-grayish or brownish pellicle. 



540 ASIATIC CHOLERA. 

By thus taking together the morphological and biological characters, 
it is possible usually on the second or third day to determine whether 
the intestinal contents of a suspected case does or does not contain the 
bacillus of Asiatic cholera. 

The cholera bacillus, both in the dejecta and in pure cultures, is 
readily stained by the ordinary aniline dyes. The results of the intro- 
duction of considerable quantities of cholera bacillus cultures into the 
gastrointestinal canal of animals have abundantly proven the causative 
relation of the bacillus to the disease. 1 

1 For the details of his researches on Asiatic cholera, see Koch's report, " Arbeiten 
a. d. kaiserlichen Gesundheitsamte," Bd. 3, 1887. 



YELLOW FEVER 



The Skin is of a yellow color from the presence of bile pigment, and 
may be mottled by eccbymoses. 

The Heart is of a pale or brownish-yellow color. Its muscular fibres 
are the seat of fatty degeneration. 

The Lungs are congested. 

The Stomach often contains the characteristic black fluid which is 
vomited during life. Its mucous membrane is congested, softened, and 
sometimes eroded. 

The Intestines are dark-colored, often distended with gas, and some- 
times contain blood. 

The Liver in the earlier stages of the disease may be intensely con- 
gested. More frequently it contains but little blood, is of a light-yellow 
color, and the hepatic cells are infiltrated with coarse granules and fat- 
globules. The gall bladder is contracted and contains but little bile. 

The Spleen shows no marked changes. 

The Kidneys present the lesions of the intense form of parenchyma- 
tous nephritis. 

While its mode of occurrence and the character of its symptoms and 
lesions afford a strong presumption that yellow fever is an acute infec- 
tious disease, none of the various studies which have been made upon 
its etiology have as yet revealed the presence of any micro-organism to 
the action of which it can be fairly attributed. 



TTJBEEOTJLOSIS. 



Persons are said to have tuberculosis when there is going on, in some 
part of their body, an inflammation accompanied with the growth of 
tubercle bacilli. 

It is also possible that persons may have tubercle bacilli in the blood 
and tissues without any inflammation, but of this we have no actual 
knowledge. 

In the experimental production of tuberculosis in animals, the inoc- 
ulation of pure cultures of the bacillus is followed by inflammatory 
changes at the point of inoculation, and then the infection of other 
parts of the body through the blood-vessels or the lymphatics. In the 
tissues thus infected inflammatory changes take place. It seems, there- 
fore, that the tubercle bacilli act as the direct cause of the inflammation. 
It has been found, however, that the spread of the bacilli from the point 
of inoculation is very decidedly influenced by the environment and mode 
of life of the animal, and that some kinds of animals are much more 
susceptible to the infection than are others. 

Inhuman beings, cases of direct local inoculation have been reported, 
but they are very rare. 

There seems to be no doubt that the bacilli can be introduced into 
the alimentary canal by infected milk and meat. It is still uncertain, 
however, how often such a mode of infection really takes place. 

The ordinary way for tubercle bacilli to be introduced into the human 
body seems to be by the air inspired into the lungs. 

Tuberculosis occurs most commonly in the form of a tubercular in- 
flammation affecting some one part of the body — "localized tubercu- 
losis." Such a localized tuberculosis may retain throughout the char- 
acters of a local inflammation; it may be accompanied by the clinical 
evidences of systemic infection; it may give rise to the successive devel- 
opment of tubercular inflammation in other parts of the body; it may 
give rise to a sudden development of tubercular inflammations in many 
parts of the body at the same time. 

It seems possible that such localized tubercular inflammations may b( 
due to the presence of the tubercle bacillus acting as a local irritant. 



TUBERCULOSIS. 543 

More frequently, however, it is necessary that a traumatism, or some 
other cause of inflammation, should set up an inflammation to which 
the tubercular character is given by the growth of the bacillus. 

The development of secondary tubercular inflammations may be due 
either to simple infection with the bacilli or to the action of fresh causes 
of inflammation. 

If there is a sudden formation of miliary tubercles in many parts of 
the body at the same time, the patient is said to have " general miliary 
tuberculosis.'"' 

Such a general infection may be caused by the diffusion through the 
body of bacilli derived from a local tuberculosis, such as tubercular 
phlebitis or arteritis, or from the breaking into a vessel of a tubercular 
lymph gland, or by the inhalation into the lungs of large numbers of 
bacilli. 

The hereditary constitution, the mode of life, the climate, all have 
a decided effect in rendering each individual more or less liable to tuber- 
cular infection. 

The method by which human beings transmit tuberculosis seems to 
be largely by means of the dried sputa. 

The forms of inflammation which are excited by or accompany the 
tubercle bacillus are the exudative and the productive. 

The inflammations run an acute, subacute, or chronic course. 

The lesions which we regularly find are: 

1 . Miliary tubercles. 

2. Diffuse inflammation of various kinds, with cheesy degeneration 
of the inflammatory products. 

3. The ordinary products of inflammation — pus, fibrin, serum, epi- 
thelium, granulation tissue, and connective tissue. 

Associated with all these lesions we find the tubercle bacilli. 

1. Miliary Tubercles. — These are small nodules, of irregularly sphe- 
roidal shape, the smallest hardly visible to the naked eye, the largest as 
large as a pea. The smaller ones are gray and semi-transparent; the 
larger are opaque, whitish or yellow, especially at their centres. 

Miliary tubercles do not all have the same structure. 

Some are composed of amorphous granular matter, of degenerated 
lung tissue, and of epithelial cells and pus. 

Some are composed of a tissue resembling granulation tissue. 

Some are composed of tubercle tissue, alone or associated with other 
inflammatory products (Figs. 44 and 128). 

The term " tubercle tissue " is employed to designate an inflammatory 
product which somewhat resembles granulation tissue. It is composed 
of a basement substance and of cells. The basement substance is deli- 
cate and finely granular, and contains round and oval nuclei. This base- 
ment substance has a reticulated arrangement, and in the spaces of the 



544 



TUBERCULOSIS. 



reticulum are polyhedral uucleated cells. There may also be present 
the large nucleated bodies called giant cells. These giant cells, although 
apparently all formed in the same way by the fusion of a number of 
smaller cells, yet do not always present exactly the same appearance. 
Some of them seem to form part of, and to be continuous with, the base- 
ment substance; others are separated from the basement substance, and 
look like large cells contained in the meshes of the basement substance. 
In some tubercle tissue the basement substance, in others the polyhedral 
cells, in others the giant cells are predominant (Figs. 42 and 43). 

Such tubercle tissue is arranged in the form of small spheroidal 
bodies — tubercle granula— and of a diffuse tissue. So that a ki tuber- 
cular" miliary tubercle is composed of one or more tubercle granula 




-\ 



V ; mm 




Fig. 216.— Tubercle Bacilli, with Pus Cells, in Sputum. 
The bacilli stained with f uchsin. 



and of diffuse tubercle, to which may be added other inflammatory pro- 
ducts. 

All miliary tubercles may undergo cheesy degeneration, or, more 
rarely, be changed into connective tissue. 

The miliary tubercles formed of amorphous granular matter or of in- 
different round-celled tissue are most common in acute general tuber- 
culosis. The miliary tubercles formed of well-defined tubercle tissue are 
most completely developed in localized tuberculosis. 

Tubercle tissue infiltrates and replaces connective tissue; it fills cavi- 
ties, and it projects from free surfaces. It contains but very few blood- 
vessels, and when it infiltrates a tissue the vessels of that tissue become 
obliterated. There is often associated with it a proliferation of the en- 
dothelial cells of the arteries or an obliterating endarteritis. 



TUBERCULOSIS. 545 

2. Diffuse Inflammation with Cheesy Degeneration of the Inflamma- 
tory Products. — This form of lesion is found in the large tubercular 
masses in the brain, in the mucous membrane of the bronchi, in the 
large flat tumors of the serous membranes, and in the diffuse, cheesy 
infiltration of the kidneys, the ureters, bladder, prostate, testicle, and 
uterus. The constant feature of the lesion is the development of an in- 
different round-celled tissue, which rapidly undergoes cheesy degenera- 
tion. Imbedded in this tissue there may be tubercle granula. When 
the lesion is far advanced, the degenerative changes may involve all the 
inflammatory products, so that we find no formed elements, nothing but 
a diffuse, caseous mass. In the earlier stages of the lesion, the indifferent 
round-celled tissue and the tubercle granula are readily demonstrated. 

3. Pus, fibrin, serum, epithelial cells, connective tissue, and indif- 
ferent tissue are all found in varying quantities, either separately or to- 
gether, in those parts of the body where the tubercular lesions have been 
developed. 

The Tubercle Bacilli are slender, filamentous bacteria (Fig. 216), vary- 
ing in length from one-fourth to one-half the diameter of a red blood- 
cell. They may contain spores, which give them a beaded appearance, 
and are sometimes slightly curved. It is possible, but very difficult, to 
see them when they have not been stained. Morphologically they very 
closely resemble the bacilli of leprosy and some other forms of filamen- 
tous bacteria. They differ from most similarly formed bacilli in the 
tenacity with which they retain the color after staining, although the 
bacilli of leprosy have this same property. It is, however, the effect of 
the living bacilli upon the organism, when introduced into it under 
favorable conditions, which furnishes the only absolute proof of their 
identity. 

The tubercle bacilli are present in the characteristic lesions of almost 
all cases of local and general tuberculosis. But there are apparently ex- 
ceptional cases of typical tuberculosis in which the most careful exami- 
nation fails to reveal the bacilli. This apparent absence of the bacilli 
is probably due either to their disappearance as the process grows older, 
or to some unknown changes which interfere with the ordinary staining 
procedures. 

The number of bacilli which are present in the lesions is subject to 
great variations. They are most abundant in the walls and contents of 
phthisical cavities, and in tubercle tissue which is undergoing cheesy 
degeneration and disintegration. In these situations they may be found 
in myriads, forming sometimes a large part of the disintegrated mass. 
They are found in cells and scattered among them. Sometimes they 
are present in considerable numbers in the giant cells of miliary tuber- 
cles. In the dense, firm, chronic miliary tubercles they are not com- 
monly present. In the acute general tuberculosis of children they are 
44 



546 TUBERCULOSIS. 

often present in enormous numbers, particularly in the lungs. They 
may be found in tubercular inflammation in any part of the body, and 
have been seen in the blood. The bacilli are almost constantly found in 
the sputa of phthisical patients, and their presence sometimes affords 
valuable diagnostic aid in early stages or obscure forms of the disease. 

METHODS OF STAINTN"G THE TUBERCLE BACILLI. 

In Fluids. — The most reliable and useful of the numerous methods 
which are employed for staining the tubercle bacilli is EhrlicWs or some 
modification of this. For the examination of fluids, such as sputum, 
etc., the material should be spread in a thin layer on a cover-glass, dried 
in the air, and then passed thrice through the flame (see page 96). The 
staining fluid is prepared by making (1) a saturated solution of anilin 
oil in distilled water; this is done by adding about five per cent of the 
oil, and shaking vigorously and filtering through a moistened filter. To 
this clear filtrate should be added (2) a sufficient quantity of a satu- 
rated alcoholic solution of fuchsin to give the fluid a dark, almost opa- 
lescent appearance (the exact amount of the stain is not important). 1 
The prepared cover-glass is floated — specimen side down — on this color- 
ing fluid, and gently boiled from three to five minutes. 

The entire specimen is thus completely stained, tubercle bacilli, tis- 
sue elements, and other bacteria which may be present, all in the same 
way. The next step is to remove the color with acid from all the struc- 
tures which may be intermingled with the tubercle bacilli; the latter, 
owing to the tenacity with which they retain the color, being but slightly 
affected. This is done by dipping the cover-glass into an aqueous solu- 
tion of twenty-five-per-cent nitric acid, and shaking it about for a few 
seconds. The acid may be even a little more dilute than this. ♦Under 
the influence of the acid, the specimen on the cover-glass loses its red 
color and becomes gray or colorless. It is then thoroughly rinsed in 
three or four successive portions of alcohol, and finally in water. By 
this manipulation the red color may be to a slight extent restored. 

Care should be taken not to expose the specimen too long to the 
action of the acid, because then the bacilli may be also partially or com- 
pletely decolorized. A little experience will enable the experimenter to 
judge of the proper time for the action of the acid. 

The specimens may be studied in water with the use of a high-power 
lens — preferably an oil immersion — and the Abbe condenser, or they 
may be dried in the air and mounted in balsam. 

Inasmuch as not infrequently some other bacteria besides the tubercle 
bacilli retain a slight red color, it is" well, after the specimen is rinsed 

1 This stain should be freshly prepared, as it does not usually keep well for more 
than a few days. 



TUBERCULOSIS. '547 

in water, to float the cover-glass for a few minutes in a dilute aqueous 
solution of methylin blue, which will replace the red color in all of the 
bacteria except the tubercle bacilli, thus forming a marked color contrast 
between them. 

Various other aniline dyes may be used instead of the fuchsin, and 
there are various minor modifications of the process which are often em- 
ployed; but, on the whole, for routine sputum examinations we recom- 
mend the method here given. 

In Sections. — Thin sections of tubercular tissue which have been 
hardened in alcohol are stained in the same way, except that instead of 
hastening the process by heating, which is apt to shrivel the sections, 
they must lie in the dye for from twelve to twenty-four hours. After 
decolorization by acid and dehydration by alcohol, the sections are 
cleared in oil of cloves and mounted in balsam. In specimens prepared 
in this way, the bacilli stand out as sharply defined slender rods or fila- 
ments on the uncolored or but slightly tinted background (Fig. 129). 

Other dilute acids besides nitric acid may be used for decolorization, 
such as hydrochloric. This is sometimes desirable in examining delicate 
tissues, since the nitric acid often causes shrinkage and distortion in the 
specimen. A one-per-cent alcoholic solution of hydrochloric acid is 
suitable for this purpose. 

For purposes of simple recognition of the bacilli in specimens, it 
seems to the writer usually better to have no color in the preparation 
other than that which the tubercle bacilli possess. But it is often con- 
venient to demonstrate the nuclei of the cells at the same time, and this 
may be accomplished by staining afterwards with some color which will 
contrast with that of the bacilli, such as Bismarck brown or methyl 
blue. 

Cultures. — The tubercle bacillus grows readily in artificial cultures 
at the temperature of the body, on blood-serum, also on agar to which ten 
per cent of glycerin has been added, and on boiled potatoes, provided 
that they be sealed in tubes so that the surfaces may remain moist. It 
forms on the surfaces of the culture dry, scaly, usually not very volumi- 
nous grayish masses. 1 

1 Bibliography. — Aside from the standard works on general pathology, the reader 
may consult, for an account of the earlier literature and investigations on tuberculosis 
up to 1869, the monograph of Waldenburg, " Die Tuberculose," Berlin, 1869. The 
announcement of the discovery of the Bacillus tuberculosis by Koch was made in the 
Berliner Klin. Wochenschrift, 1882, No. 15. A most elaborate and valuable article 
on the same subject by Koch is contained in the " Mittheilungen aus dem Kaiserlichen 
Gesundheitsamte," vol. ii. 

The very voluminous literature on the subject of the tubercle bacillus which has 
accumulated since 1882 is for the most part scattered through the German, English, 
and French journals. It may be best obtained by consulting files of the Index Medi- 
cus of dates since April, 1882. 



LUPUS. 



This form of inflammation most frequently occurs in the skin of the 
face, but also in the mucous membrane of the mouth, pharynx, con- 
junctiva, vulva, and vagina. The lesion consists of small, multiple 
nodules of new-formed tissue, somewhat resembling granulation tissue, 













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--'•< 


>* v . 


■y'j'~ 


8jP^^lyy>'v%''' v J 


'? ■>& 


«• '■'■'; '■*•""' *'»-' -'";'"••-''=" 


**■"•* /»| 




r^>» 


? | U^ y i~^£ 




V-?-. - '^^ 


'.• *rn*.^''*%*"*^ 




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1111 


its* 

lip 


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PS? 






Fig. 217. — Lupus of Face. 



in the cutis or mucosa and submucosa. By the formation of new nodules 
and a more diffuse cellular infiltration of the tissue between them, the 
lesion tends to spread, and by the confluence of the infiltrated portions 
a dense and more or less extensive area of nodular infiltration may be 



lupus. 549 

formed. There may be an excessive production and exfoliation of epi- 
dermis over the infiltrated area, or an ulceration of the new tissue. 

Microscopical examination shows the lesion to consist in the forma- 
tion of tissue composed of small spheroidal cells, intermingled with vari- 
able numbers of larger, so-called epithelioid cells and cell masses, and, 
in many cases, with giant cells (Fig. 217). In some cases, a well- 
marked reticulum is present between the new cells, and these are often 
grouped in masses around the blood-vessels. In some cases, there is, 
without previous ulceration, a formation of new connective tissue in the 
diseased area, and a well-marked cicatrization; in other cases, the cells 
and intercellular substance undergo a disintegration which leads to 
ulceration. 

The morphological characters of the lesion long ago led to the con- 
jecture that lupus was in reality a form of tubercular inflammation. 
This view has now become established by the numerous observations 
which show the very constant presence of the tubercle bacillus at the 
seat of inflammation. It is not unlikely, however, that in the clinical 
group of diseases called lupus there may be lesions which are not caused 
by the tubercle bacillus. More exact bacterial studies must be made 
before this point can be fully decided. 



ERYSIPELAS. 



Erysipelas is a diffuse inflammation of the skin and subcutaneous 
tissue which tends to spread, and which especially involves the lymph 
spaces and the lymph vessels. It is characterized locally by swelling of 
the tissue and a bright red color of the integument. It is regularly 
accompanied by constitutional disturbances, the most marked of which 
is fever. The morphological changes at the seat of lesion, as we see 
them after death, vary considerably in different cases and in different 
stages of the disease. The redness of the disease usually disappears 
after death. But the tissues may be swollen by the accumulation of 









Fig. 218.— Micrococci in Blood and Lymph Vessels of the Skin in Erysipelas. 

serous fluid. This fluid may be nearly transparent, or turbid from ad- 
mixture with pus cells. Pus cells may infiltrate the tissues either 
sparsely or in dense masses. Sometimes vesicles are found on the sur- 
face, or scabs; sometimes more or less of the affected region becomes 
filled with abscesses or gangrenous. In some cases we find, aside from 
the local lesions, petechias in the serous membranes, swelling of the 
spleen, and parenchymatous degeneration of the kidneys and liver. 

The researches of Fehleisen and others have shown that erysipelas is 
caused by the presence and action in the tissues of a chain coccus called 
Streptococcus erysipelatos. These bacteria are usually most abundant 
in the lymph vessels and lymph spaces along the advancing borders of 






ERYSIPELAS. 551 

the inflammatory area, but they may be contained in the blood-vessels 
(see Fig. 218). 

The Streptococcus erysipelatos is a moderately large coccus, varying, 
however, considerably in size, and may occur singly, in pairs, or in 
longer and shorter chains (see Fig. 219). It is readily cultivated artifi- 
cially, forming in gelatin tubes a series of small whitish colonies along 
the puncture line, and not fluidifying the gelatin. Its growth in gen- 
eral is slow. It forms a scarcely visible growth. At 35° C. on potatoes, 
and in beef- tea at the same temperature, it forms within twenty-four to 
forty-eight hours an abundant flocculent deposit which may cling to the 
sides of the tube. 

Inoculation of rabbits with the pure culture may induce a fairly 
typical erysipelatous inflammation, but, as these animals are not espe- 






Fig. 219.— Streptococcus erysipelatos. From a beef -tea culture. 

cially susceptible to its action, the results of inoculations are not con- 
stant. 

In its morphological and histological characters it appears to be 
identical with the Streptococcus pyogenes and Streptococcus diphtheriae. 
There appears to be much reason for believing that many forms of 
phlegmonous inflammation, and many forms at least of diphtheria and 
erysipelas, are different phases of the inflammatory process due to the 
same organism; the difference in the reaction of the tissues which 
constitute the clinical differences characteristic of the different diseases 
being due, perhaps to differences in the tissues involved, perhaps to 
variations in the characters and virulence of the germ, and perhaps to 
causes which at present we know nothing about. 

Further researches are required to fully explain the exact relation- 
ship of these at least closely allied forms of inflammation to one another 
and to the bacteria which cause them. 



PYEMIA. 



It has long been known that a certain number of persons who have 
received wounds by accident or by the hands of the surgeon may suffer 
from constitutional symptoms and develop lesions. To designate the 
condition of these patients, the terms pyaemia, septicaemia, septo-pyaemia, 
ichorrhaemia, inflammatory fever, surgical fever, traumatic fever, sup- 
purative fever, and purulent infection have been used. Attempts have 
been made to distinguish several different forms of disease and to call 
one pyaemia, another septicaemia, and so on, but these attempts have not 
proved satisfactory, and for the present it is better to include them all 
under the general name of pyaemia. 

As regards the nature of pyaemia three theories have been held : 

I. That pus is absorbed, circulates in the blood, and acts as a poison. 

II. That a chemical poison is evolved from pus and the other matters 
which are found in wounds, and that the system is poisoned by this. 

III. That bacteria are introduced into and developed in the wound, 
find their way into the blood and tissues, and there multiply (see page 
92). 

The following are the ordinary forms of the disease commonly called 
pyaemia, with the lesions : 

I. There are cases of wounds and injuries which are characterized by 
the presence of a febrile movement without any other symptoms. In 
such cases, no lesions are found except extravasated blood and portions 
of necrotic tissue, neither of which are in the condition of putrefaction. 

II. There are cases in which, in some part of the body, a portion of 
tissue is not only dead but putrefying. While the process of putrefac- 
tion is going on, the patient suffers from rigors, a febrile movement, 
great prostration, and may die. If, however, the dead tissue can be re- 
moved or the putrefactive process arrested, all the symptoms rapidly 
disappear. 

III. A very small wound may apparently introduce at once into the 
body a specific poison, as in dissecting wounds. There are swelling and 
redness about the wound, and inflammation of the lymphatic vessels and 
glands in its neighborhood. Later all the neighboring tissues become 



PYEMIA.. 553 

involved in an unhealthy inflammation; there may be infarctions in the 
viscera, a large soft spleen, and parenchymatous degeneration of the liver 
and kidneys. 

IV. There is a large number of cases which it is difficult to classify. 
They are the ordinary hospital cases of compound fracture and surgical 
wounds. After the death of these patients, there is a considerable va- 
riety in the post-mortem appearances. 

1. There are cases in which there are no recognizable lesions. 

2. There are cases characterized by early post-mortem decomposition; 
post-mortem staining of the tissues; congestion of the lungs, stomach, 
intestines, and kidneys; extravasations of blood in the serous membranes; 
swelling of the solitary and agminated glands in the small intestine; 
swelling of the spleen and parenchymatous degeneration of the liver and 
kidneys. 

3. In some cases there are localized inflammations. The joints, the 
connective tissue around the joints, the pleura, the pericardium, the 
peritoneum, the pia mater, and the connective tissue in different parts of 
the body maybe inflamed. These local inflammations are of a purulent 
character, except in the serous membranes, where the principal in- 
flammatory product may be fibrin. 

4. There are cases in which the veins in the neighborhood of the 
wound contain softened, puriform thrombi; there are no infarctions in 
the viscera, but there maybe inflammation of the joints and serous mem- 
branes. 

5. In other cases the veins contain thrombi; there are infarctions and 
abscesses in the viscera; local inflammations of the joints and serous 
membranes may be present or absent. The thrombi are formed regularly in 
the veins near the wound, but they may be situated in veins at a distance, 
and sometimes, although infarctions and abscesses are present, no throm- 
bus can be discovered. The veins may be distended by the thrombi or 
only contain small coagula. The different kinds of thrombi, and the 
varieties of emboli and infarctions which they produce, are described in 
the article on Thrombosis, page 55. 

Y. Prolonged Suppuration. — There is first a wound, or a bruise, or 
an idiopathic suppurative inflammation. This original focus of in- 
flammation continues to suppurate for a long time, then successive ab- 
scesses are formed in different parts of the body, the patients lose flesh 
and strength, and die in a condition of extreme emaciation. After 
death, abscesses are found in different places, but not in the viscera. 
There are no thrombi nor infarctions. There may be bronchitis or 
broncho-pneumonia. The liver, spleen, and kidneys are often the seat 
of waxy degeneration. 

VI. Spontaneous Pymmia. — Under this name we include a group of 
cases which resemble ordinary pyaemia in their symptoms and lesions, 
45 



554 



PYEMIA. 



but are of obscure etiology. There is no wound, fracture, or abscess to 
account for them, but they present the same symptoms and the same 
lesions as the ordinary cases of pyaemia. 

Bacteria in Pycemia. — In a very large proportion of cases of pyaemia, 
micrococci, scattered and in colonies, are found in various parts of the 
body (Fig. 220). The species which have been most frequently identi- 
fied are the Streptococcus pyogenes and the Staplrylococcus pyogenes. 
These bacteria, when present, apparently stand in a causative relation to 




^m 










Fig. 220.— Micrococci in Zooglcea Colonies in the Fibrinous Exudation of Pyemic Pleurisy. 



the disease. But until we have a more precise conception of what we 
mean by the name pyaemia, it is difficult to speak with much definite- 
ness of its causative factors. 

If we regard pyaemia as an acute infectious disease, caused by the 
entrance into the body of certain bacteria, then it is probable that the 
bacteria most frequently concerned are those species above mentioned, 
Avhich are also the most common causative factors in suppurative inflam- 
mation. 



ANTHRAX. 



Synonyms. —Splenic fever; Malignant pustule; Charbon, Carbuncle. 

This disease, which is much more common in the lower animals, 
especially the herbivora, than in man, is of infrequent occurrence in the 
United States. It is induced in man by the accidental inoculation with 
the Bacillus anthracis, which causes the disease in the lower animals. 
This may occur through the agency of flies which have been feeding on 
animals infected with this disease, by handling their carcasses or hides, 




Fig: 221.— Bacillus anthracis growing in the Blood Vessels of the Liver of a Mouse in- 
occjlated with a pure culture of the bacillus. 



or in other ways. There may be in man local lesions in the skin, in the 
form of papules, pustules, or a phlegmonous inflammation, with oedema 
and lymphangitis. The disease may remain local, or general infection 
may occur. In some cases, there is apparently no external lesion. 

When general infection occurs, the post-mortem appearances vary. 

Decomposition, as is usual in acute infections, generally sets in early. 
The blood is frequently not much coagulated and dark in color. Hsem- 



556 ANTHRAX. 

orrhages and ecchymoses are frequently found in the serous and mucous 
membranes, and in various other parts of the body. 

The lungs may show small haemorrh ages and oedema, and the bronchi 
may be deeply congested. The pleural cavities may contain serum. 
The intestines may exhibit the lesions of the so-called intestinal mycosis 
(see page 338). The bronchial and other lymphatic glands may be swol- 
len. The spleen may be swollen, very dark in color, and soft, sometimes 
almost diffluent. 

The bacillus which causes the disease may be found, usually in large 
numbers, in the spleen and in the capillary blood-vessels, especially in 
the liver, lungs, kidneys, and intestine (see Fig. 221). 

The Bacillus anthracis is from 5 to 20 ju long, and about 1 jj. broad, 
and is often slightly curved (see Fig. 2<J2). The ends are not rounded, 




Fig. 222.— Bacillus anthracis. 

and they often hang together end to end, forming thread-like structures. 
They develop spores outside of the body which are very invulnerable to 
the action of the ordinary germicidal agents and to heat. They are im- 
mobile. 

They are readily cultivated outside of the body, and, when thus puri- 
fied, their inoculation into various species of animals produces the dis- 
ease, and in the blood of the diseased animals multitudes of the bacilli 
are found, showing their proliferation in the blood-vessels and else- 
where. They are of especial interest and importance, because we know 
more of their life history than of almost any other of the bacteria, and 
because it was this bacterium which was first absolutely demonstrated to 
be the cause, and the only cause, of a well-defined disease in man. 1 

For the literature of the relations of the Bacillus anthracis to this disease, etc., 
see Koch, " Mitth. a. d. Kaiserlichen Gesundheitsamte," Bd. 1, p. 49 et seq. 



LEPKOSY. 



Lepra (Leprosy). — This form of inflammation is characterized by the 
development of nodular and sometimes diffuse masses of tissue, consist- 
ing of larger and smaller cells of various shapes— spheroidal, fusiform, 
and branched — the whole somewhat resembling granulation tissue. The 
new tissue is most frequently formed in the most exposed parts of the 
skin, as the face, hands, and feet, but it may occur in the skin of any 
part of the body. It is formed more rarely in the subcutaneous connec- 
tive tissue, in intrafascicular connective tissue of nerves, in the viscera, 
and in the mucous membranes. The mucous membranes most frequently 




Fig. 223.— The Bacilli of Leprosy. 
Stained with fuchsia. From a nodule in the skin. 



affected are those of the eye, nose, mouth, and larynx. The nodules 
may be very small or as large as a walnut, and may be single or joined 
together in groups or masses. The tissue of the part in which the new 
formation occurs may be atrophied and replaced, or may remain inter- 
mingled with the leprous tissue, or it may be hypertrophied. The nod- 
ules may persist for a long time without undergoing any- apparent change, 
or they may soften and break down, forming ulcers; but ulceration, ex- 
cept in the mucous membranes, is said usually to occur as the result of 
injury or unusual exposure. The leprous tissue may change without 
ulceration into cicatricial tissue, or cicatrization may follow ulceration. 
Various secondary lesions and disturbances of nerve function are 



558 LEPROSY. 

associated with the formation of leprous tissue in the nerve and central 
nervous system, but these we cannot consider here. 

In all the primary lesions of lepros}^, bacilli are said to be present, 
mostly in the cells, and particularly in the larger spheroidal forms, but 
sometimes free in the intercellular substance. The bacilli have been 
found in the skin, mucous membrane of the mouth and larynx, in peri- 
pheral nerves, in the cornea, in cartilage, in the testicles, and in lymph 
nodes. Sometimes the cells contain but few bacilli, but they are fre- 
quently crowded with them. The bacilli are from 4 to 6 ju long and 
very slender, being usually less than 1 pi in thickness. They are some- 
times pointed at the ends, and sometimes present spheroidal swellings, 
which seem to indicate the formation of spores (Fig. 223). They are 
capable of spontaneous movement. In their comportment towards stain- 
ing agents, as well as in general morphological characters, they con- 
siderably resemble the Bacillus tuberculosis. They may be stained with 
fuchsin or gentian violet by the ordinary method, or by the method 
employed for staining the tubercle bacillus. 

According to Neisser, the lepra bacillus may be artificially cultivated 
on blood-serum and on boiled eggs. 

The reasonable conjecture that the Bacillus leprae causes the lesions 
of leprosy depends as yet largely upon the constancy of their occurrence 
in the disease, and upon their relations to the cells of the new growth. 



GLAJSDEES— FARCY. 



These names are given to two varieties of the same disease. The dis- 
ease originates in the horse and occurs in men by contagion. According 
to some authors, it may be idiopathic in the human subject. 

In the horse we find four varieties of the disease: chronic and acute 
glanders, chronic and acute farcy. 

1. Chronic Glanders. — The disease begins in the mucous membrane 
of the nose. Small, whitish nodules, composed of small rouud cells, are 
formed in the mucous membrane. These nodules soften and ulcerate. 
The same nodules maybe found in the larynx, trachea, and bronchi. 
The ulcerations may remain superficial, or they may extend and attack 
the subjacent cartilage and bone. Nodules of the same kind may be 
found in the lungs. 

' 2. Acute Glanders. — There is the same formation of nodules, which 
softeu and ulcerate; but they are accompanied with an intense inflam- 
mation of the nasal mucous membrane, and the disease runs a rapid 
course. 

3. Chronic Farcy. — The lymphatic glands and vessels become en- 
larged, and nodules are formed in the skin, lungs, and other viscera. 
The glands become cheesy or soften and suppurate. The cutaneous 
nodules soften and suppurate. 

4. Acute Farcy. — There are the same lesions of the lymphatics, and 
nodules and abscesses are found in the skin. There are also nodules in, 
and inflammation of, the nasal mucous membrane, and the disease runs 
an acute course. 

In man, the disease occurs in an acute and a chronic form, but does 
not exactly resemble any of the varieties of the disease in the horse. 

The acute disease runs a rapid and malignant course. The skin may 
be covered with a pustular eruption. Furuncles, carbuncles, and ab- 
scesses are found beneath the skin and in the muscles. Nodules are 
found in the nasal mucous membrane, the lungs, kidneys, testes, spleen, 
and liver. The joints may be inflamed, and there may be osteomyelitis. 

The disease may begin at a single point, so that it may be mistaken 
for a carbuncle or a gangrenous erysipelas. Graefe gives a case which 



560 GLANDERS FAKCY. 

began as an acute exophthalmos, and the nature of the disease was not 
ascertained until after death. In this case there were nodules in the 
choroid coat of the eye. 

The chronic form of the disease is still more difficult of diagnosis. 
The nodules grow very slowly, are hard, and may occur in groups or like 
a string of beads. The nodules may soften and form chronic ulcers. 

A slender bacillus, called Bacillus mallei, has been proven to be the 
cause of glanders both in man and animals. They occur either scattered 
or in masses in the areas of fresh inflammation, and have been found in 
the blood of affected individuals. They have been repeatedly artificially 
cultivated, and successful inoculations practised with the pure cultures 
upon animals. The bacilli grow at the temperature of the body on 
blood-serum and on potato pulp. 1 

1 Consult Loeffler, " Arbeiten a, d. Kais. Gesundheitsamte/' Bd. 1 7 1886, 



HTDEOPHOBIA. 



The lesions which have been found in this disease are not constant 
nor are they characteristic. Though well marked in some cases, they 
are but very slightly developed in others. 

The lesions, when present, are apt to be most marked in the medulla 
oblongata and pons, but they may be present in the cord. They consist 
of small haemorrhages, and accumulation of leucocytes about the blood- 
vessels in the perivascular lymph spaces and of thrombi in the smaller 
blood-vessels. 

While there is much reason for believing that hydrophobia is due to 
the introduction into the body of some special form of micro-organism, 
and while the recent researches of Pasteur and others have brought to 
light many interesting and important facts regarding the general nature 
and distribution in the body of the infectious agent, nothing is yet 
definitely known about the particular organism which induces the dis- 
ease. 

46 



THE MALARIAL FEVERS. 



The characteristic lesions of malarial poisoning are certain changes 
in the blood, the spleen, and the liver. 

In the more intense and acute form of malarial poisoning, the blood 
contains numerous particles of black or brown pigment, which are either 
free or imbedded in cells resembling the white blood-cells and the endo- 
thelium of the blood-vessels (see Fig. 164). After death, this pigment 
is found in the blood-vessels throughout the body, but is most abundant 
in the blood-vessels of the liver and spleen. These organs are then usu- 
ally of large size and of a peculiar brown or black color. 

In some of these severe cases, there are also extravasations of blood 
from the mucous membranes, and in their substance. There may also 
be general jaundice. 

In the milder and more protracted cases of malarial poisoning, the 
composition of the blood is altered, and the patients may become pro- 
foundly anaemic. The spleen may become the seat of chronic interstitial 
inflammation with pigmentation (see Fig. 174). The liver may exhibit 
the changes of chronic interstitial hepatitis. 

The attempts to establish a causative relationship between the various 
forms of bacteria which from time to time have been found in the bodies 
of persons who are the victims of malarial poisoning, and the symptoms 
and lesions of the disease, have all been unsuccessful. 

On the other hand, a large number of careful studies by various ob- 
servers have led to a strong presumption that the disease is due, not to a 
vegetable, but to an animal organism which is very constantly found in - 
the blood of affected persons. 

In brief, the facts upon which this presumption rests are as follows: 
The blood of those suffering from malarial poisoning may contain one 
or more of the structures which are shown in Fig. 224. 

1. Inside of the red blood-cells may be found colorless bodies, some- 
times occupying a small part, sometimes nearly filling the cell. These 
bodies may or may not contain pigment granules. They may exhibit 
amoeboid movements (a and b). They are called the amoeboid bodies. 



THE MALARIAL FEVERS. 



563 



2. Colorless discoidal bodies, usually a little larger than the red blood- 
cells, which contain pigment particles, sometimes scattered irregularly, 
sometimes grouped towards the centre. These are believed by some ob- 
servers to be later developmental stages of the amoeboid bodies, which 
have increased in size at the expense of the red blood-cell. A grouping 
of the pigment granules indicating segmentation is sometimes seen in 
these bodies. These are called the incysted bodies (c). 

3. Bodies, about the size of a red blood-cell, which are composed of a 
congeries of irregularly rounded structures grouped about a central mass 
of pigment. These are called segmenting bodies or rosettes (d). 

4. Smaller isolated or clustered structures which are apparently the 




Fig. 224.— Plasmodium Malarle in the Blood. 
a, unpigmented amoeboid body in a red blood cell; 6, pigmented amoeboid body; c, colorless 
discoidal body with pigment; d, segmenting body; e. fragments of segmenting body; / and g, 
crescentic bodies; h, flagellate body. a. b. d, e, /, g, are drawn from specimens of malarial blood 
prepared by Dr. Walter James; c and h are drawn after sketches by Dr. James. 



result of the breaking apart of the segmenting bodies as seen at e. Often 
called spores. 

5. Crescentic bodies containing a central mass of pigment (/and g). 

6. Bodies, smaller than a red blood-cell, which are actively mobile and 
are furnished with one or more flagellae at one side — h, flagellate form. 
These are the main forms which have been described. 

The amoeboid forms are apt to occur in the acute stages of the dis- 
ease, the crescentic forms in the chronic stages. The segmenting bodies 



564 THE MALARIAL FEVERS. 

are apt to be present immediately before or during the chill; the pig- 
mented amoeboid bodies, according to James, are present at all times, but 
are most numerous during the paroxysm. The amoeboid forms disappear 
shortly after the administration of quinine, while the crescentic bodies 
often persist for a considerable time under the same conditions. 

Whether these various bodies are developmental forms of the same 
organism or not has not yet been fully established, as artificial cultiva- 
tions have not been made. 

The organism, which apparently belongs among the protozoa, may be 
most appropriately called the Jus mat o zoo n of malaria. It is, however, 
often called the Plasmodium malarise. 

Whatever its etiological significance or its life history, its discovery 
in the blood, even with our present knowledge, since it is unknown ex- 
cept in malarial disease, is of great diagnostic value in doubtful cases. 

Method of Examination. — The fresh blood taken from a finger prick 
may be examined in thin layers with one-twelfth oil immersion. Or the 
blood may be spread in a very thin layer on a cover-glass, dried, passed 
through a flame, and then stained as in the ordinary mode of bacterial 
examination with fuchsin or methylin blue (see page 96). The stained 
specimens may be mounted and preserved in balsam. 1 

1 For a more detailed account of the ha?matozoon of malaria and literature, consult 
James, " Micro-organisms of Malaria." Proceedings New York Pathological Society, 
January 25th, 1888. 



DISEASES CHAEAOTERIZED BY ALTERA- 
TIONS IN THE COMPOSITION OF 
THE BLOOD. 



There is a group of diseases in which the essential lesion seems to be 
an alteration in the composition of the blood, although in some members 
of the group other lesions are also present. This group embraces Chlo- 
rosis, Pernicious Anaemia, Addison's Disease, Leukaemia, and Pseudo- 
Leukaemia. 

CHLOROSIS. 

In many cases of chlorosis the only lesion is the change in the com- 
position of the blood. 

The volume of the blood may be diminished, the red blood-globules 
contain less haemoglobin, the number of red blood-cells is diminished; 
there are present red blood-cells, some of which are larger and some 
smaller than the normal cells. 

In a few cases there is also present a congenital smallness of the 
aorta. 

PERNICIOUS ANJEMIA. 

In this disease the same changes in the blood exist as in chlorosis, and 
there may also be a moderate increase in the number of the white blood- 
cells. 

There is often fatty degeneration of the walls of the heart and of the 
arteries. 

There may be thrombosis of the pulmonary artery. 

The same changes in the marrow of the bones are found as in leu- 
kaemia. 

There may be ecchymoses in different parts of the body. 

ADDISON'S DISEASE. 

This name is applied to a disease characterized by a peculiar pigmen- 
tation of -the skin, certain changes in the suprarenal capsules, and a 



566 ALTERATIONS IN THE COMPOSITION OF THE BLOOD. 

diminution in the number of red blood-cells. The patients become very 
ansemic, but are not emaciated. They suffer from cerebral symptoms, 
great prostration, syncope, and derangements of the functions of the 
stomach and intestines. 

The pigmentation of the skin is the symptom which has especially 
attracted attention. The change in color usually begins and becomes 
most marked in those parts of the skin which are not covered by the 
clothing, or are naturally darker colored. The rest of the skin after- 
wards changes color, but not uniformly, white patches being left. The 
color is at first a light yellow or brown; this becomes darker until it is 
of a dark greenish, grayish, or blackish brown. The mucous membrane 
of the tongue, lips, and gums may be pigmented in the same way. 

Under the name of Addison's disease different observers have de- 
scribed cases in which the symptoms and bronzed skin existed without 
disease of the suprarenal capsules; cases in which the bronzed skin was 
the only lesion, and cases in which the suprarenal capsules were diseased 
without symptoms or bronzed skin. 

We hardly know as yet what are really the characteristic lesions of 
the disease. 

The Skin. — The discoloration of the skin is due to deposit of yellow- 
ish-brown pigment in the deeper layers of the epidermis, especially in 
the layer covering the papillae, and less constantly in the connective tis- 
sue of the cutis. 

The Brain. — Pigmentation of the gray matter, acute meningitis, 
chronic meningitis, and distention of the ventricles with serum have been 
observed. 

The Heart. — The muscular fibres may be the seat of fatty degenera- 
tion. 

The Sympathetic Nerves may show a variety of changes apparently 
due to chronic inflammation, especially the nerves which are in contact 
with the suprarenal capsules. 

TJie Suprarenal Capsules. — The most common lesion of these bodies 
is a tubercular inflammation resembling that which occurs in the lym- 
phatic glands. 

The suprarenal capsules are large, hard, and nodular; less frequently 
of normal size or atrophied. On section, they are found to contain 
cheesy masses, surrounded by zones of gray, semi-translucent tissue. 
Later the cheesy masses may become calcified or they may soften and 
break down. 

The grayish zones are composed of tubercle tissue, granulation tissue, 
and connective tissue. 

Other cases have been described in which the suprarenal capsules 
were the seat of carcinoma, or of fatty or waxy degeneration. The supra- 
renal capsules in some cases appear normal. 



ALTERATIONS IN THE COMPOSITION OE THE BLOOD. 567 

The Blood exhibits the same changes as exist in pernicious anae- 
mia. 

LEUKAEMIA (LEUCOCYTH^EMIA). 

This disease is characterized by a persistent and progressive increase 
in the number of white blood-cells in the blood, accompanied by altera- 
tions of varying amount in the spleen, lymph glands, and bone marrow. 
Sometimes one, sometimes another of these organs is especially in- 
volved. Not infrequently other internal organs, lungs, liver, kidneys, 
etc., are more or less densely infiltrated with leucocytes, either diffusely 
or in nodular form. The lymphatic tissue of the gastro-intestinal canal 
may be in a condition of hyperplasia. 

Ecchymoses in the serous and mucous membranes, or severe haemor- 
rhages on slight provocation, and fatty degeneration of the heart and 
kidneys, frequently complicate leukaemia. Aside from various other 
foreign chemical substances which may exist in the blood in leukaemia, 
there are very frequently found in the blood, marrow, spleen, liver, etc., 
after death, elongated octahedral crystals, called Charcot's crystals, which 
are believed to be formed by a combination of phosphoric acid with some 
organic base. 1 

For a detailed description of the lesions of the different parts of the 
body in leukaemia, see chapters on Blood, Spleen, Lymph Glands, Bones, 
etc. It does not fall within the scope of this work to consider the various 
theories as to the probable causes of this disease, which is very obscure 
and but little understood. 2 • 

PSEUDO-LEUKJEMIA (HODGKIN'S DISEASE). 

In pseudo-leukcemia, which is very closely related to leukaemia, the 
anatomical changes in the organs are apparently identical with those of 
leukaemia, but there is no increase in the number of leucocytes in the 
blood. Of the internal organs the lymph glands are most apt to be 
specially affected in pseudo-leukaemia. 

1 For literature of Charcot's crystals, consult Zenker, Arch, fur klin. Medicin 
Bd. 18, p. 125, 1876. 

2 For literature of leukaemia and pseudo-leuksemia, consult BircJi-HirscJifeld, 
11 Lehrbuch der path. Anatomie," 2d ed., Bd. 2, p, 146. For general consideration 
of the relation of certain diseases of the blood to the blood-forming organs — spleen, 
lymph glands, etc. — see Cohriheim's " Vorlesungen tiber allgemeine Pathologie," 
vol. i. 



SCOKBUTTTS— PTTBPUKA— H.EMATOPHILIA. 



SCORBUTUS (SCURVY). 



This disease appears to result from imperfect nutrition under condi- 
tions which cannot be considered here, and whose immediate cause we 
do not understand. The lesions are variable, the most prominent being 
extravasation of blood in the skin, subcutaneous tissue, and muscles; 
swelling and ulceration of the gums. Small and sometimes extensive 
haemorrhages are apt to occur in the mucous membranes and on serous 
surfaces. Small ulcers may form in the mucous membranes. Fatty 
degeneration of the heart, liver, and kidneys is not uncommon. The 
spleen may be large and soft. No constant characteristic changes have 
been discovered, either in the blood-vessels or the blood, which would 
satisfactorily account for the extravasations and other lesions. 

The body is apt to decompose early. The skin may be mottled 
with small and large purple, blue, brown, or blackish spots produced 
by degenerative changes in the extravasated blood in the cutis. Some- 
times ulcers are produced by the perforation of effused blood on to the 
surface. 

The joints may be inflamed, may contain serum or blood. Rarely 
the haemorrhages are followed by destruction of the cartilages and ends 
of the bones. 

Very rarely there is haemorrhage between the periosteum and bone, 
and in the bone itself, producing softening and destruction of the bone, 
and separation of the epiphyses. The sternal ends of the ribs are the 
most frequent seat of this change. 

PURPURA HEMORRHAGICA (MORBUS MACULOSUS). 

This disease is characterized by the occurrence of ecchymoses in the 
skin, mucous and serous membranes. Haemorrhages, particularly from 
the mucous membranes, may be very severe and even fatal. The caus( 
of the disease is unknown. 



SCORBUTUS PURPURA — ELEMATOPHILIA. 569 

ELEMATOPHILIA (HEMORRHAGIC DIATHESIS). 

This disease consists in a liability to haemorrhage on the slightest 
provocation, and is dependent upon some constitutional peculiarity 
which is unknown to us. It is frequently hereditary. An unusual 
thinness of the intima of the arteries has been noticed in some cases, 
and other changes have been described, but there are no constant lesions 
associated with the haemorrhages, as yet discovered, which would satis- 
factorily explain their occurrence. The haemorrhages may be traumatic 
in origin, or they may occur spontaneously from the mucous mem- 
branes. 



GOUT. 



The characteristic lesion of gout is the deposit of urate of soda in the 
articular cartilages, the ligaments of the joints, the ears, and the eye- 
lids. 

The most frequent situation is the metatarso-phalangeal joint of the 
great toe. The cartilage may be intiltrated or incrusted with the 
deposit. 

A very important feature of gout is that patients with the gouty dia- 
thesis are especially liable to derangements of digestion and to certain 
chronic inflammations, such as chronic inflammation of the arteries, 
chronic bronchitis, and chronic nephritis. 



DIABETES. 



It would be expected that so common and well marked a disease as 
saccharin diabetes should be characterized by definite lesions, but this 
is not the case. The changes which we find after death are accidental, 
or the results of the disease. No characteristic lesions have yet been 
discovered. 

The Brain may appear to be entirely normal; it may be congested; 
there may be an increase of serum; the convolutions may be shrunken; 
there may be meningitis; there may be dilatation of the blood-vessels, 
small extravasations of blood around the vessels, enlargement of the 
perivascular spaces, and alterations in the perivascular sheaths, and 
nervous matter bounding the cavities; there may be tumors at the base 
of the brain. 

' The Spinal Cord may present dilatation of the blood-vessels; dilata- 
tion of the central canal; changes in the gray matter of the anterior 
oornua. 

The Lungs. — There maybe pleurisy, bronchitis, broncho-pneumonia, 
lobar pneumonia, gangrene of the lung, chronic pulmonary phthisis. 

The Heart is often small; there may be chronic endocarditis. 

The Stomach and Intestines. — The stomach may be dilated, its walls 
may be thickened, there may be hemorrhagic erosions of the mucous 
membrane. In the intestines there may be tubercular ulcers or ente- 
ritis. 

The Liver and the Spleen show no marked changes. 

The Pancreas may be atrophied; it may contain abscesses. 

The Kidneys may be enlarged; they may be the seat of parenchyma- 
tous or diffuse nephritis; there may be glycogenic degeneration of the 
epithelium of Henle's loops. 

The Blood. — In a few cases fat has been found in the blood and fat 
emboli in the vessels of the lungs. 

A considerable number of autopsies are recorded in the Transac- 
tions of the Pathological Society of London, vol. xxxiv., p. 328, and in 
French's monograph on "Diabetes." 



SUlSrSTBOKE. 



During the hot summer months, cases of sunstroke are of frequent 
occurrence in New York. The persons affected are, for the most part, 
adult male laborers, usually of intemperate habits. 

It is necessary to separate from the cases of sunstroke proper, when 
the patient is attacked while exposed to the heat of the sun, the cases 
of exhaustion from heat and fatigue, which may occur as well in the 
house. 

The patients who are seriously affected by sunstroke exhibit, during 
life, an intense heat of the skin, convulsions, and coma. Death in many 
cases soon ensues. In other cases, the symptoms are more protracted. 

After death, decomposition sets in very early, owing to the state of 
the weather. In autopsies which I have made within two hours after 
death, the increased heat of the skin was still maintained. 

The Brain and its membranes were in some cases congested, in others 
not. Sometimes there was an increased amount of serum beneath the 
pia mater; sometimes there were small and thin extravasations of blood 
beneath the pia mater, and between the pia and dura mater. 

In the other viscera there were no lesions except those due to the 
condition of coma existing before death. The lungs and kidneys were 
frequently congested. 

In the cases in which cerebral symptoms are protracted for a number 
of days, the lesions of meningitis have been found after death. 

Attention has been called by Dr. H. 0. Wood, Jr., to the rigid con- 
dition of the wall of the heart after death, but this rigidity is certainly 
not present in all cases. 






DEATH FROM BURNING. 



Death may be caused by the inspiration of smoke and flame; by 
drinking of hot fluids; by the direct contact of flame or hot substances 
with the external surface of body. It may be due to the direct effect of 
the agents, to secondary affections of the viscera, or to the exhaustion 
produced by long-continued inflammation and suppuration. 

The entire body may be burned to a coal or completely roasted, or 
only a larger or smaller area of the skin be burned. 

We find the burned skin divested of epidermis and presenting a 
peculiar red, hard, parchment-like appearance. If the patient has 
lived some time, this is replaced by a suppurating surface. Or there 
are small, bladder-like elevations of the epidermis. The base of these 
blisters is red, and they are surrounded by a red zone, or suppuration 
may have commenced. 

These appearances cannot be produced by heat applied to the skin 
after death. 

The Brain may be congested, cedematous, or softened. More fre- 
quently it is normal. 

The Larynx and Trachea ma} 7 be congested and the seat of croupous 
inflammation. There may be oedema of the glottis. 

The Lungs may be congested and cedematous, or hepatized, or the 
seat of pysemic infarctions. There may be pleurisy. . 

Inflammation of the per it oneum is not very infrequent. There may 
be swelling of the solitary and agminated glands of the small intestine. 

The duodenum may be the seat of perforating ulcers and the mucous 
membrane of the entire gastro-intestinal canal may be congested. The 
Liver, Spleen, and Kidneys may be the seat of parenchymatous degen- 
eration or of pyaemic infarctions. 



DEATH FEOM LJGHTNING. 



Persons who are struck by lightning may die instantly; or may con- 
tinue for several hours comatose or delirious, and then either die or 
recover; or they may die after some time from the effects of the burns 
and injuries received. 

The post-mortem appearances are very variable. Sometimes there 
are no marks of external violence or internal lesions. Sometimes the 
clothes are burnt and torn, while the skin beneath them is unchanged. 
Usually there are marks of contusion and laceration, or ecchymoses, or 
lacerated, punctured wounds, or fractures of the bones, or superficial or 
deep burns. The track of the electric fluid may sometimes be marked 
by dark-red arborescent streaks on the skin. Fractures are rare. 

The internal viscera may be lacerated and disorganized from light- 
ning. 






DEATH FROM SUFFOCATION— ASPHYXIA. 



By suffocation we understand that condition in which air is prevented 
from penetrating into the lungs without direct pressure on the larynx 
or trachea. The interruption of the function of respiration which is 
thus brought about induces the condition known as asphyxia. Many 
deaths from drowning and strangulation take place in this way. 

The methods in which the supply of air may be cut off from the lungs 
are very various. The mouth and nose may be closed by the hand, by 
plasters and cloths, by wrapping up the head in cloths, by covering the 
face with earth, hay, grain, etc. Foreign bodies may be introduced into 
the mouth, pharynx, and larynx. Blood may pass into the trachea from 
an aneurism or from a wound. The glottis may be closed by inflamma- 
tory swelling. Matters which are vomited may lodge in the ]arynx. 

On the other hand, injury or disease of the medulla oblongata, or par- 
alysis, or spasm of the muscles of respiration from drugs, tumors press- 
ing upon the air passages, or diseases of the lungs themselves, may induce 
asphyxia. 

EXTERNAL INSPECTION. 

The body should be examined for marks of violence, the cavities of 
the mouth and nose for foreign substances. 

The face may be livid and swollen or present a natural appearance. 
The conjunctiva may be congested and ecchymotic. There may be 
small ecchymoses on the face, neck, and chest. The mouth often con- 
tains frothy blood and mucus. The tongue may be protruded. 

INTERNAL EXAMINATION. 

The Brain and its membranes may be congested, or anasmic and. 
oedematous, or unchanged. 

The Blood throughout the body is unusually dark-colored and fluid. 

The Larynx may contain foreign bodies which have produced the 
suffocation. The mucous membrane of the larynx, trachea, and bronchi 
is congested and sometimes ecchymotic. These passages contain frothy 
blood and mucus. 

The Lungs are usually congested and oedematous, but sometimes do 



576 DEATH FBOM SUFFOCATION ASPHYXIA. 

not differ from their ordinary appearance. There may be small patches 
of emphysema near the surface of the lungs. Sometimes, especially in 
infants, small ecchymoses are found in the costal and pulmonary pleura. 

The Heart usually presents its right cavities full of blood, its left 
cavities empty; but to this there are frequent exceptions. 

The Abdominal Viscera are usually congested. 

DEATH FROM STRANGULATION— HANGING. 

Strangulation is effected by the weight of the body in hanging, by 
pressure on the neck with the hands or by some other object, or by con- 
striction of the neck with a cord or ligature of some kind. Death is 
usually produced by asphyxia, or by asphyx a combined with the effect 
of the cutting-off of the blood supply to the brain by pressure on the 
large vessels of the neck. In some cases of hanging, death ensues as a 
result of fracture or dislocation of the cervical vertebrae. 

EXTERNAL INSPECTION. 

The face may be livid and swollen, the eyes prominent, the lips 
swollen, and the tongue protruded. These appearances are, however, 
often absent. Erection of the penis, ejaculation of semen, and evac- 
uation of faeces and urine are frequently observed. 

In most cases, marks are left upon the neck by the objects whic] 
have directly produced the strangulation. 

In cases of hanging, the mark about the neck varies considerably in 
position, direction, and general characters, depending upon the kind of 
ligature employed, the time of suspension, 'period after death at which 
the observation is made, etc. The most common mark left by a cord 
about the neck is a dry, dense, brownish furrow, whose breadth corre- 
sponds but in a very general way with the diameter of the cord. In 
some cases, according to Tidy and others, there may be no mark at all 
if the hanging is quickly accomplished with a soft ligature and the body 
cut down immediately after death. There may be abrasions and ecchy- 
moses of the skin at the seat of ligature. 

In cases of strangulation by the fingers, the marks on the neck may 
correspond in a general way to the shape of the fingers. 

The application of the same forces immediately after death may pro- 
duce the same marks as when death is induced by them. 

INTERNAL EXAMINATION. 

The Brain and its membranes may be congested, or there may be 
extravasation of blood, or there maybe no abnormal appearances. 

The Neck. — In some cases there is effusion of blood beneath the 
ligature, rupture of the cervical muscles, fracture of the os hyoides and 



DEATH FROM SUFFOCATION ASPHYXIA. 577 

cartilages of the larynx, fracture and dislocation of the cervical ver- 
tebrae, rupture of the internal vertebral ligaments and of the inner and 
middle coats of the carotid arteries. Similar changes may be produced 
in the dead body by the use of great violence. In death from asphyxia, 
the lesions are similar to those described above. In some cases, for ex- 
ample, where death has occurred from fright or shock, the results of 
post-mortem examination are entirely negative. 



DEATH FROM DROWNING. 

In examining the bodies of persons who have been drowned it is 
necessary to bear in mind a number of questions which may arise : 
Whether the person came into the water alive or dead ? How long a 
time has elapsed since death ? Whether the person committed suicide, 
or was drowned by accident, or was murdered ? These questions are to 
be solved sometimes certainly, sometimes with probability, sometimes not 
at all, by the post-mortem examination. Persons dying in the water, to 
which condition the term drowning is commonly applied, may die from 
asphyxia, from exhaustion, from fright or syncope, from diseases of the 
heart, apoplexy, injuries, etc. While in the majority of cases asphyxia 
is a predominant or important factor in death by drowning, the condi- 
tions under which death occurs are so apt to be complex that in the 
minority of cases only are the lesions of pure asphyxia found after death, 
while in most cases the bodies present the more or less well-marked 
lesions of asphyxia together with those indicative of complicating con- 
ditions. There are no post-mortem conditions which alone are abso- 
lutely characteristic of drowning, and it is only by considering all the 
facts elicited by the autopsy together that any just conclusion can be 
arrived at. It should always be borne in mind, moreover, that even the 
most characteristic of the evidences of drowning are apt to be modified 
or to disappear as decomposition goes on. 

EXTERNAL INSPECTION. 

Post-mortem rigidity usually sets in early, sometimes immediately 
after death. Decomposition goes on, especially in summer, with un- 
usual rapidity in bodies which have been removed from the water. 
Frequently, but by no means constantly, the peculiar roughening of 
the skin, known as goose skin (cutis anserina), is found, but this may 
occur after death from other causes. A light, lathery froth, either 
white or blood-stained, is frequently seen about the mouth and nostrils 
within twelve to twenty-four hours after removal of the body from the 
water, but it may be absent, and may be seen after death from other 
causes. After the body has lain for several hours in the water (twelve 
to twenty-four), the thick skin of the palms of the hands and soles of 
47 



578 DEATH FROM SUFFOCATION ASPHYXIA. 

the feet may become macerated and thrown into coarse wrinkles, just 
as it may after prolonged soaking during life, or in a dead body thrown 
into the water. The penis and nipples may be retracted and the 
scrotum shrunken, but this is not constant nor characteristic. 

If the person has struggled in the water and clutched at objects 
within his reach, there may be evidences of this in excoriations of the fin- 
gers or in the presence of sand, weeds, etc., under the nails or grasped 
in the hands. 

External marks of injury, bruises, etc., should be sought for, since 
persons in diving, or on being thrown into the water with homicidal 
intent, may have died from the violence, and not, strictly speaking, 
from drowning. It should also be borne in mind in such complex cases 
that injuries, not in themselves fatal, may, when the body is in the 
water, prove so on account of the inability of the person to rescue him- 
self or gain time for recovery from the injury, and that then the strug- 
gle for breath may be but slight, and the more prominent signs of 
drowning but little marked. 

INTERNAL EXAMINATION. 

The Brain. — Congestion of the brain and its membranes is found 
only in a small proportion of cases. 

The Blood, when death occurs from asphyxia, is usually fluid 
throughout the body and of a dark color, as in asphyxia from other 
causes. 

The Air Passages. — In persons who die from asphyxia, the mucous 
membrane of the larynx, trachea, and bronchi is usually congested, and 
the air passages contain a variable quantity of bloody or mucous froth. 
In persons dying in the water from other causes than asphyxia, these 
appearances are absent. Foreign substances from the water, such as 
sand, weeds, etc., or matters regurgitated from the stomach, may find 
their way into the air passages during the act of drowning or as a post- 
mortem occurrence. Thus in bodies washed about on the bottom, sand 
or mud may get into the air passages for a certain distance, from the 
mechanical action of the water. 

The Lungs in typical cases are distended, so that they fill the thorax 
and cover the heart. The increased size is due partly to congestion, 
partly to the presence of the fluid in which the person was drowned, 
which is often inspired during the act of drowning, and partly to the 
distention of the air vesicles with air. While in cases of drowning in 
which there is a struggle, and water is breathed in, the lungs contain 
more or less fluid, this may, as a result of decomposition, find its way 
in greater or less quantity into the pleural cavities by transudation, leav- 
ing the lungs comparatively empty. It should be remembered, how- 
ever, that a considerable quantity of reddish fluid may collect in the 



DEATH FROM SUFFOCATION ASPHYXIA. 579 

pleural cavities under other conditions than drowning, as a post-mortem 
change, by transudation from the blood-vessels and other adjacent 
tissues. 

The Heart, — In those who die from asphyxia, the right cavities are 
usually filled with fluid blood, while the left cavities are empty. But 
where death is due to complex causes this may not be the case. 

The Stomach. — The fluid in which the person was drowned, sometimes 
mixed with sand, weeds, etc., may be swallowed during the act of 
drowning. Sand may wash for a short distance into the oesophagus 
after death, in bodies washing about the bottom. 

The Abdominal Viscera may be congested in persons who die from 
asphyxia. 

In persons dying from syncope, shock, etc., we may find no lesions. 
When the death is partly due to asphyxia, and partly to other causes, 
the conditions will vary in various ways, which need not be described in 
detail here. 

In important cases of doubtful drowning, it is desirable to carefully 
collect and save some of the fluid from the lungs and stomach for micro- 
chemical examination, since the identification of these fluids with those 
in which the person was presumably drowned will often give certainty 
to an otherwise doubtful case. 

For the detailed consideration of the anatomical diagnosis of drown- 
ing, the changes which bodies dead from drowning undergo from decom- 
position, and the factors bearing on the question of suicide, homicide, 
etc., we refer to works on medical jurisprudence. 1 

1 Tidy, "Legal Medicine," vol. ii., 342-373. Guy and Ferrier, "Forensic Medi- 
cine," 274-285. 



DEATH FEOM POISONING. 



In cases of suspected poisoning which may possibly have a medico- 
legal bearing, the examination should be made with extreme care and 
thoroughness. The inspection of the body and the examination of all 
the viscera should be thorough and detailed. Every appearance should 
be noted at the time and nothing left to the memory. It is well to have 
an assistant record the observations as they are made. The disposition 
of the parts and organs in jars should also be noted at the same time. 

It is important to remember that many poisons destroy life without 
producing appreciable lesions, and also that many cases of sudden death 
occur, not due to poisons, and without any discoverable cause. 

In bodies which are exhumed for examination, the tissues may be 
so changed by decomposition that it is impossible to say whether lesions 
have or have not existed. In such cases, the careful and separate pre- 
servation of the viscera and other parts for chemical examination is 
often all that can be done. For directions for preserving tissues and 
organs for the chemist in medico-legal cases, see Part I. (p. 35). 

SULPHURIC ACID. 

The effects of this poison vary with the amount taken and with its 
strength. Death usually takes place in from two to twenty-four hours 
after the taking of the concentrated acid. A case of death within an 
hour is recorded. When the poison is less concentrated, or its effects 
less intense, the patient may survive for months. 

The skin of the face about the mouth may be blackened and charred 
by the acid. The mouth and pharynx are of a grayish or blackish color, 
or are covered with a whitish layer, while the deeper tissues are reddened. 
Sometimes these regions escape the action of the poison. 

The larynx, trachea, and lungs are sometimes acted on, softened and 
blackened by the accidental passage of the acid into them. This may 
even take place when the acid does not pass into the oesophagus. 

The cesophagus seldom escapes. It is grayish or blackish colored, 
softened, and the mucous membrane comes off in shreds. If life is pro- 



DEATH FROM POISONING. 581 

longed, cicatrices and strictures are formed. The stomach may contain 
a blackish, pulpy fluid, due to the action of the acid on mucus, blood, 
etc. It is coated on its internal surface with a black, sticky layer, beneath, 
which the mucous membrane is reddened. The mucous membrane may 
be blackened in patches or stripes. The organ may be contracted and 
the mucous membrane corrugated. Sometimes perforation takes place, 
and the acid blackens and softens the adjoining viscera. In protracted 
cases, cicatrices are formed and the organ is contracted. If the poison 
is dilute, there may be only the lesions of chronic gastritis. 

The blood is sometimes thickened, syrupy, acid, and may form thrombi 
in the vessels. 

The body may be partially preserved from decomposition, owing to 
the action of the acid upon the tissues. 

Fatty degeneration of the renal epithelium is mentioned by some 
authors. 

The solution of indigo in sulphuric acid, commonly known as sulphate 
of indigo, produces the same lesions as sulphuric acid, and also stains the 
tissues with which it comes in contact of a dark-blue color. It is stated 
that an indigo blue tint is often found in the mucous membranes after 
poisoning by pure sulphuric acid. 1 



NITRIC ACID. 

Death may occur very soon after the taking of the poison, but does 
not usually occur for several hours, and may not take place for several 
days or weeks. 

The surface of the mucous membrane of the mouth, pharynx, and 
oesophagus is covered with yellow eschars wherever the acid has touched 
it. Beneath and around the eschars the tissues are congested and red. 
The poison may be introduced into the oesophagus without acting on the 
mouth. The stomach contains a viscous, sanguinolent. yellow or green- 
ish fluid. The mucous membrane is congested, red, swollen and 
softened, ecchymotic. It is rarely perforated. The duodenum may be 
inflamed, and the inflammation extend to its peritoneal coat. The rest 
of the intestines usually escapes the action of the acid. 

The larynx is very frequently acted on by the acid. There are yel- 
low eschars, congestion and swelling of the mucous membrane, sometimes 
oedema of the glottis. The trachea may be inflamed and the lungs con- 
gested. 

If the patient survives the first effects of the poison, the lesions of 
chronic inflammation, cicatrization, and contraction may be found at a 
later period. 

1 Woodman and Tidy, "Forensic Medicine and Toxicology," ed. 1877, p. 237. 



582 DEATH FEOM POISONING. 

The acid nitrate of mercury, if taken in a concentrated form into the 
stomach, may produce the same lesions as nitric acid. 

HYDROCHLORIC ACID. 

In fatal cases, death occurs on the average in about twenty-four 
hours. The lesions are in general similar to those produced by sul- 
phuric and nitric acids, except that the eschars are usually of a whitish 
color at first, becoming, after a time, discolored and disintegrated. It 
is also more common to find false membranes on the inflamed surfaces. 

OXALIC ACID. 

In fatal cases, death may occur within ten minutes (in one case in 
three minutes) or may be delayed for two or three weeks. The period 
of death does not depend, as do in general the symptoms, upon the 
amount and concentration of the poison. 

The mucous membrane of the mouth, pharynx, and oesophagus is 
usually white and shrivelled, and easily peeled off, and may be covered 
with brownish vomit from the stomach. The oesophagus may be much 
contracted. The stomach is usually contracted and contains a dark- 
brown, acid, mucous fluid. The mucous membrane of the stomach may 
be pale, soft, and easily detached, sometimes looking as if it had been 
boiled in water. Sometimes it is red and congested; sometimes blackened 
and gangrenous; sometimes peeled off in patches. Perforation is of 
rare occurrence. If life be prolonged, the whitened condition of the 
mucous membrane is succeeded by congestion and inflammation. The 
small intestines may be inflamed. Inflammation of the pleura and peri- 
toneum, and congestion of the lungs, are of occasional occurrence. In 
some cases of death from oxalic acid there are no well-marked lesions. 

Potassium oxalate produces the same lesions as oxalic acid. 

TARTARIC ACID. 

This acid is seldom used as a poison, but in large doses may prove 
fatal. The lesions in the cases observed were redness and inflammation 
of the mucous membrane of the gastro-intestinal canal. 

POTASH, SODA, AND THEIR CARBONATES. 

These substances are not commonly used as poisons with suicidal or 
homicidal intent, but may be taken by mistake. They may cause death 
in a few hours, or life may be prolonged for several weeks. 

The mucous membrane of the mouth, pharynx, oesophagus, and 
stomach is softened, swollen, congested, and inflamed, or may be peeled 
off. It may be blackened from local changes in the blood. The mucous 
membrane of the larynx and trachea may also be swollen and inflamed. 



DEATH FROM POISONING. 583 

If life is prolonged for some time, cicatrices and strictures of the 
oesophagus and stomach are apt to be produced as a result of the repara- 
tive inflammation. 

AMMONIA. 

The vapor of strong ammonia may cause death from inflammation of 
the larynx and air passages. The strong solution of ammonia produces 
lesions similar to those of potash and soda. The larynx, trachea, and 
bronchi are frequently inflamed, and may be covered with false mem- 
branes. Fatal inflammation of the rectum and colon has been produced 
by an enema of strong solution of ammonia. 

POTASSIUM NITRATE. 

Accidental poisoning sometimes occurs from large doses of this salt. 
In the observed cases, there were intense congestion and inflammation of 
the stomach and intestines, and in one case a small perforation of the 
stomach. 

For the effects of several infrequently employed salts of the alkalies 
and alkaline earths, which for the most part produce simple inflamma- 
tion of the gastro-intestinal canal, we refer to special works on toxi- 
cology. 

PHOSPHORUS. 

Poisoning by phosphorus is much more common in France and Ger- 
many than in this country. Some of the forms of rat poison, of which 
this is a frequent ingredient, and the ends of matches are common media 
for its administration. It is more often used with suicidal than homici- 
dal intent. 

The post-mortem appearances vary according to the length of time 
which elapses before death, which may be from a few hours to several 
mouths. 

If death takes place in a few hours, the only lesions may be those 
produced by the direct local action of the poison. The mouth, pharynx, 
and oesophagus usually escape. The stomach may be only slightly red- 
dened, or there may be patches of inflammation and erosion. The con- 
tents of the stomach are often mixed with blood, and may have the 
peculiar smell of phosphorus. There may be little bits of wood present 
when the poison has been taken from the heads of lucifer matches. It 
is said that the mucous membrane of the stomach may emit a phos- 
phorescent light in the dark. 

If death does not ensue until after several days, the lesions are more 
marked. The body is usually jaundiced. There may. be ecchymosis 
beneath the pericardium, pleura, and peritoneum, in the lungs, the kid- 



584 DEATH FROM POISONING. 

neys, the bladder, the uterus, the muscles, and the subcutaneous con- 
nective tissue, and bloody fluid in the visceral cavities. 

The heart and voluntary muscles, the walls of the blood-vessels, and 
the endothelium of the air vesicles of the lungs may be in the condition 
of fatty degeneration. The blood is usually dark and fluid. 

The stomach sometimes presents no very striking changes. There 
may be small circumscribed spots of inflammation, erosion, or gangrene, 
and occasionally perforation. The most constant change is a granular 
degeneration of the cells which fill the gastric follicles. In consequence 
of this, the mucous membrane appears thickened, opaque, of white, gray, 
or yellow color. 

The small intestine appears normal or is congested. 

The liver is found in different degrees of parenchymatous and fatty 
degeneration, and is often stained yellow from the jaundice. It is usu- 
ally increased in size, and of a grayish, grayish-yellow, or light-yellow 
color, unless stained by the bile. Less frequently the centres of the acini 
are congested, or the entire liver is congested, or there are small haemor- 
rhages in the liver tissue. The liver may be soft, flabby, and smaller 
than normal. In the interstitial tissue of the liver and along the 
branches of the portal vein there may be marked infiltration with small 
spheroidal cells. 

The kidneys often present parenchymatous and fatty degeneration of 
the epithelium. The mesenteric glands may be soft and swollen. 

ARSENIC. 

This poison is very frequently employed with suicidal iutent. Death 
may occur in a longer or shorter time from the direct irritative effects of 
the poison upon the gastro-intestinal canal, with the symptoms which 
usually accompany the ingestion of irritant poisons; or it may occur 
with symptoms of collapse, or coma, or shock; or the symptoms may 
resemble those of cholera. The average time of death in acute fatal 
cases is about twenty hours, but death has occurred in twenty minutes, 
and has been prolonged for two or three weeks. 

The month, pharynx, and oesophagus may be inflamed, but are more 
frequently unaltered. The stomach may be empty or contain mucus 
mixed with blood. The arsenic, in substance, may be found adherent to 
the mucous membrane or mixed with the contents of the organ. It has, 
in rare cases, been found incysted in the stomach in considerable quan- 
tity. When invisible to the naked eye, a microscopical examination of 
the stomach contents will not infrequently reveal characteristic crystals 
of arsenious acid or some of its compounds. The stomach may be con- 
tracted and its mucous membrane corrugated. The entire inner surface 
may be red and inflamed, or there may be patches or streaks of inflam- 



DEATH FROM POISONING. 585 

mation or deep congestion. The inflamed and congested patches may 
be thickened and covered with false membrane mixed with larger and 
smaller particles or masses of the poison. Ulceration, perforation, and 
gangrene are rare. Blood may be extravasated into the mucosa and 
submucosa, and with the congestion give the mucous membrane a very 
dark-red or brown appearance. Frequently the mucous membrane is 
studded with small petechias Sometimes the arsenic is converted in the 
stomach into the yellow sulphide. There may be acute gastritis, even 
when the poison is absorbed by the skin or otherwise, and not introduced 
into the stomach. Taylor mentions a case in which the coats of the 
stomach were thickened and gelatinous, but not congested. The epi- 
thelium of the gastric glands may undergo granular and fatty degenera- 
tion. 

The entire length of the intestine may be congested and inflamed, 
but the action of the poison does not usually extend beyond the duode- 
num. In some cases, the solitary follicles, Peyer's patches, and mesen- 
teric glands are swollen. Inflammation of the bladder and peritoneum,, 
and congestion and oedema of the brain, have been observed, but are 
neither frequent nor in any way characteristic. 

Fatty degeneration of the muscles, liver, kidneys, blood-vessels, and 
vesicular epithelium of the lungs may be produced in arsenical poison- 
ing. 

Alterations in the spinal cord indicative of acute myelitis have been 
described by Popon as occurring in dogs poisoned with arsenious acid. 1 

The walls of the stomach and intestines and other parts of the body 
may be preserved from decomposition for a long time after death by 
arsenical poisoning. 

It should always be borne in mind, in examining cases of suspected 
arsenical poisoning, that death may be produced by arsenic and its com- 
pounds without any appreciable lesions. While in general it may be 
said that in the cases in which no lesions are discovered death has been 
rapid, the death may be delayed in such cases until long after a period 
at which, in other cases, marked inflammatory changes have occurred. 

Compounds of arsenic, such as the chloride and sulphide, and the 
arsenite (Scheele's green; Paris green), are sometimes used for suicidal 
purposes, and produce lesions similar to those of arsenious acid. Paris 
green is a favorite article in New York, particularly among Germans, 
for suicidal purposes. It is usually taken in considerable quantities, and 
is often found in the stomach after death. 2 

1 Popon, ' ' Ueber die Veranderungen im Riickenmarke nach Vergiftung mit Arsen," 
etc. Virch. Arch., Bd. 93, p. 351. 

2 It is advisable, in cases of suspected arsenic poisoning, particularly if the body 
have lain for some time, as in exhumations, to preserve not only all of the internal 
organs entire for the chemist, but also portions of the muscles (back, thigh, arm, and 



586 DEATH FROM POISONING. 

CORROSIVE SUBLIMATE. 

The raucous membrane of the mouth and throat may be swollen, in- 
flamed, or have a grayish-white appearance. The oesophagus may be 
swollen and white, or congested, or unaltered. The mucous membrane 
of the stomach is usually congested or inflamed, or there may be patches 
of softening, ulceration, or gangrene. Perforation is of rare occurrence. 
Small ecchymoses in the mucosa are not uncommon. Sometimes there 
is little or no change in the stomach. Sometimes the mucous membrane 
of the stomach is slate-colored from the deposition of metallic mercury 
from the decomposed salt. The intestines may appear normal, or there 
may be patches of congestion aud ecchymosis. 

The larynx and trachea may be congested. The kidneys may show 
parenchymatous and fatty degeneration of the epithelium. 

LEAD. 

The different preparations of lead may prove fatal, either from the 
immediate effect of large doses or from the gradual effects of repeated 
small doses. Although there may be marked symptoms during life, the 
post-mortem lesions are few and variable. 

Large doses may produce acute gastritis, and sometimes a whitening 
of the mucous membrane. The intestines are generally contracted, and 
there may be fatty degeneration of the renal epithelium; very frequently 
there are no appreciable lesions. 

In chronic lead poisoning, the intestines may be contracted, the vol- 
untary muscles flabby and light-colored, or partially replaced by connec- 
tive tissue, and there may be chronic meningitis. 

COPPER. 

Acute poisoning by salts of copper is not very common, but it is of 
occasional accidental occurrence, and the salts are infrequently used with 
suicidal intent. The sulphate and acetate are the most important salts 
in this respect. Soluble salts of copper may be formed in the use of 
copper cooking utensils, and accidents most frequently occur in this 
way. 

The post-mortem appearances are somewhat variable. The pharynx 

abdomen), and also one of the long bones, preferably the femur, since arsenious acid 
and its compounds are quite diffusible, and may be present in proportionately larger 
quantity in other parts than in the gastro-intestinal canal. It is desirable to save the 
whole of the internal organs, and to weigh the muscle and bones as well as the whole 
body at the autopsy, in order that the calculations of the chemist, in case arsenic be 
found, may rest upon a definite basis, and be as little as possible dependent upon 
estimates, whose value may be questioned by lawyers should the case come into the 
courts. 



DEATH FEOM POISONING. 587 

and oesophagus may be somewhat inflamed or unchanged. The mucous 
membrane of the stomach and intestines may be inflamed, ulcerated, or 
gangrenous, and perforation and peritonitis may occur. The mucous 
membrane may have a diffuse greenish color, or particles of the salt may 
be found adhering to it. 

TARTAR EMETIC. 

This preparation of antimony may prove fatal when administered in 
a single large dose or in repeated small doses. The post-mortem lesions 
are not constant. In cases of chronic poisoning there are usually no 
appreciable lesions. 

In cases of acute poisoning there may be evidence of acute inflamma- 
tion of the oesophagus, stomach, intestines, and peritoneum. Sometimes 
the stomach exhibits no lesions, while the intestine is involved. The 
larynx and lungs may be deeply congested. 

VEGETABLE IRRITANTS. 

Aloes, colocynth, gamboge, jalap, scammony, savin, croton oil, colchi- 
cum, veratria, hellebore, elaterium, and turpentine. 

All these drugs may produce poisonous effects. The post-mortem 
lesions are congestion, inflammation, and sometimes ulceration of the 
gastro-intestinal mucous membrane; but these lesions are sometimes 
present and sometimes absent. 

CANTHARIDES. 

This substance may be given in powder or tincture. The entire 
length or only a portion of the alimentary canal may be congested or 
inflamed. There may be patches of gangrene of the mucous membrane 
of the stomach. When the poison was taken in substance, a microscopi- 
cal examination of the contents of the alimentary canal or of the mucous 
membrane may reveal the glistening green and gold particles of the fly. 

The kidneys, ureters, and bladder may be congested and inflamed. 
There is sometimes congestion of the brain and its membranes. 

OPIUM. 

The post-mortem appearances in persons who have died from opium 
poisoning are inconstant and not characteristic. Congestion of the 
brain and its membranes, with serous effusion in the membranes and 
ventricles, and congestion of the lungs, are changes occasionally seen, 
but they are frequently entirely absent, and when present are not char- 
acteristic of death from this poison. 



588 DEATH FROM POISONING. 

POISONOUS FUNGI. 

The action of these substances varies greatly, and the post-mortem 
appearances are inconstant and not characteristic. In general, when 
any lesions are present, they are those of gastro-intestinal irritation or 
of venous congestion, or both. 

Microscopical examination may reveal characteristic fragments of 
fungi in the contents of the alimentary canal. 

HYDROCYANIC ACID. 

This poison in fatal doses may destroy life in a very short time. The 
post-mortem appearances are inconstant and not characteristic. The 
skin may be livid and the muscles contracted. The stomach may be 
congested or normal. The most frequent internal appearances are 
those of general venous congestion. Under favorable conditions the 
odor of prussic acid may be detected in the stomach or blood or brain or 
other parts of the body. It may be absent in the stomach and present 
in other parts of the body. If the patient have lived for some time, the 
odor may be absent altogether. 

Cyanide of potassium may produce the same lesions as prussic acid, 
and there is the same inconstancy in their occurrence. 

Nitrobenzole. — This substance produces general venous congestion, 
and the odor of the oil of bitter almonds may be more or less well 
marked in the body after death. 

CARBOLIC ACID. 

When this poison is taken into the stomach, the mucous membrane 
of the mouth, oesophagus, and stomach may be white, corrugated, and 
partially detached in patches, and the edges of the affected parts may 
be hypersemic or there may be patches of extravasation. Brownish 
shrunken patches may be present about the mouth. The brain and 
meninges may be congested. There may be congestion and cedema of 
the lungs, and congestion of the liver and spleen. The blood is usually 
dark and fluid. The urine is usually of a dark or greenish color. The 
odor of the poison may be evident in the body and in the urine. 

ALCOHOL. 

The different preparations of alcohol, when taken in concentrated 
form or in large quantities, sometimes produce sudden coma and death 
in from half an hour to several hours. In acute poisoning, if death 
have followed soon after the ingestion of the poison, the body may 
resist decomposition for an unusual length of time. The stomach and 
tissues may even have a more or less well-marked alcoholic odor. The 



DEATH FEOM POISONING. 589 

stomach, and even the oesophagus and duodenum, may be of a deep-red 
color. There may be punctiform ecchymoses in the gastric mucons 
membrane. In many cases, the stomach is apparently quite normal. 
There is apt to be venous congestion in some of the internal organs, but 
this is not constant. There is frequently congestion and sometimes 
extravasation of blood in the brain and its membranes, and oedema of 
the membranes or of the brain substance, or both. There may be a 
serous effusion in the ventricles of the brain. The bladder is frequently 
distended with urine, as in other cases in which death is preceded by 
a period of unconsciousness. 

Chronic alcoholic poisoning is of a different nature. The subjects 
of it may die from some other disease, or they die after a debauch with- 
out anything else to account for their death. In the latter case there 
may be delirium tremens, or the patient dies exhausted and comatose. 
Chronic alcoholism is not infrequently mistaken clinically for meningitis. 
The post-mortem lesions are sometimes marked, sometimes absent. 
There may be chronic pachymeningitis, resulting in thickening of the 
dura mater and its close adherence to the skull. The pia mater may be 
thickened and ©edematous. The brain may be normal or oedematous or 
atrophied. The lungs are frequently congested. The heart may be 
thickly covered with fat, and its walls may be flabby and fatty. The 
stomach frequently presents the lesions of chronic gastritis. The liver 
may be cirrhotic, with or without fatty infiltration. The kidneys may 
present the lesions of parenchymatous or fatty degeneration or of chronic 
diffuse nephritis. 

It should always be remembered, however, that all or a part of the 
above lesions may be absent in the bodies of drunkards, and, further- 
more, that the same lesions may be due to other causes. 

CHLOROFORM. 

Chloroform may cause death when it is taken in fluid form into the 
stomach or when inhaled. Death from swallowing liquid chloroform is 
rare, and its immediate cause is usually uncertain. The post-mortem 
changes are variable; sometimes there are no lesions. In some cases 
there is simple reddening of the gastric mucous membrane; occasionally 
there is acute gastritis or ulceration of the mucous membrane. The odor 
of chloroform may or may not be evident. Discoloration and softening 
of the mucous membrane of the pharynx, oesophagus, and duodenum 
have been observed. There may be general venous congestion; the heart 
may be flabby. Bubbles of gas have been frequently seen in the blood, 
but this is not characteristic. Death from inhalation of chloroform is a 
not infrequent accident in surgical practice. After death from inhala- 
tion, the results of the examination are usually quite negative. 



54)0 DEATH FEOM POISONING. 

ETHER. 

The inhalation of ether occasionally causes death. The post-mortem 
examination is negative. The ingestion of fluid ether may induce in- 
flammation of the stomach. The odor of ether may be perceptible if the 
autopsy is made soon after death. 

CHLORAL HYDRATE. 

There are no characteristic post-mortem appearances after death by 
chloral. Hyperemia of the brain, and the odor of the drug, have been 
noticed. 

STRYCHNIA— NUX VOMICA. 

The post-mortem appearances after poisoning by these drugs are not 
characteristic, and are inconstant. The body is usually relaxed at the 
time of death, but the rigor mortis usually comes on early and remains 
long. There may be congestion of the brain and spinal cord, and some- 
times of the lungs and stomach. 

CONIUM, ACONITE, BELLADONNA, LOBELIA INFLATA, DIGITALIS, 

STRAMONIUM. 

These vegetable poisons are administered in their natural form of 
leaves, berries, and roots, or in tinctures,, infusions, and extracts, or in 
the form of their active alkaloid principles. 

If the leaves, berries, or seeds are given, they may be detected in the 
contents of the stomach by microscopical examination. Otherwise the 
results of autopsies are not characteristic. 

The brain and its membranes, and the lungs, may be congested. 
The stomach may present patches of congestion, inflammation, and 
extravasation, or its entire mucous coat may be inflamed, or it may 
appear normal. 

Microscopical examination of the contents of the alimentary canal 
may reveal characteristic seeds or fragments of leaves. 1 

CARBONIC OXIDE. 

This is one of the gases formed iu the burning of charcoal, and 
forms one of the ingredients of illuminating gas. The most character- 
istic post-mortem appearance is the cherry-red color of the blood, and of 
the tissues and viscera which contain blood. The presence of carbonic 
acid in the gas may obscure the bright red of the carbonic oxide by the 
dark color which it induces in the blood. 

1 Consult Guy and Ferrier, " Forensic Medicine," p. 534. 



DEATH FROM POISONING. 591 



CARBONIC ACID. 



The lesions are essentially those of asphyxia, but the brain is said to 
be more frequently congested than in asphyxia by simple obstruction of 
respiration. 

For a more detailed consideration of poisons, their effects, modes of detection, etc. , 
consult Taylor on Poisons; Maschka's " Handbuch der gerichtlichen Medicin," 
Bd. 2; Woodman and Tidy, "Forensic Medicine." Wormley's " Micro chemistry of 
Poisons " contains a series of good plates of the microscopical appearance of various 
forms of crystals of poisonous substances. 

Lesser 's "Atlas der gerichtlichen Medicin " contains a series of fine colored plates 
showing the appearance of the stomach after the action of various poisons. The 
small work of Guy and Ferrier, on " Forensic Medicine," contains in very compact 
and reliable form much^information on the general subjects treated in the foregoing 
section. 



INDEX. 



Abbe's condenser, use of, in examining 

bacteria, 99 
Abdominal cavity, examination of, in 
adults, 17, 25 
cavity, examination of, in 

children, 41 
cavity, methods of opening, 

17 
cavity, serum in, as a result 
of post-mortem changes, 18 
organs, post-mortem changes 

in, 18 
pregnancy, 462 
Abscesses, formation of, in inflammation, 
107 
of brain, 187 
Acarus scabiei, 81 
Accessory spleens, 28 
Achorion Schonleinii, 83 
Acid, carbolic, poisoning, lesions of, 588 
carbolic, preserving action of, 49 
carbonic, poisoning, lesions of, 591 
chromic, use of, in decalcifying 

tissues, 44 
hydrochloric, poisoning, lesions of, 

582 
hydrocyanic, poisoning, lesions of, 

_588 
nitric, poisoning, lesions of, 541 
nitric, use of, in decalcifying tis- 
sues, 44 
osmic, use of, in preserving tissues, 

45 
oxalic, poisoning, lesions of, 582 
picric, use of, in decalcifying, 43 
picric, use of, in preserving sedi- 
ments, exudations, casts, etc., 46 
sulphuric, poisoning, lesions of, 580 
tartaric, poisoning, lesions of, 542 
Aconite poisoning, lesions of, 590 
Acrania, 195 
Actinomyces, 83 

Acute yellow atrophy of liver, 359 
Addison's disease, lesions of, 565 
Adenoma, general consideration of, 148 
Adeno-sarcoma, 135 

Agar, use of, in cultivating bacteria, 101 
Ague-cake, 382 
Aguillula, 81 

48 



Air, presence of, in blood, air emboli, 61 
Alcohol poisoning, lesions of, 588 

use of, in preserving tissues, 44 
Alimentary canal, 310 
Aloes poisoning, lesions of, 587 
Alveolar carcinoma, 159 

sarcoma, 134 
Ammonia poisoning, lesions of, 583 
Amoeba, occurrence of, in dysenteiy, 70 
Amyelia, 209 
Amyloid degeneration, 66 

degeneration, methods of stain- 
ing tissues in, 66 
Anaemia, changes of blood in, 59 

changes of marrow cells in, 456 
effects of, on tissues and organs, 

53 
pernicious, 565 
Anencephalia, 195 
Aneurism, cirsoid, 290 

dissecting, 291 
false, 294 

miliary, of brain, 185 
of the aorta, 291 
of the blood-vessels, 292 
of the coronarv arteries, 292 
of the heart, 282 
of the heart valves, 282 
of the pulmonary arteries, 292 
spurious, 294 
varicose, 294 
Aneurismal varix, 294 
Angioma cavernosum, 145 

telangiectodes, 144 
Angiomata, general characters of, 144 
Angio-sarcoma, 133 
Anhydraemia, 59 

Aniline colors, uses of, in staining bacte- 
ria, 96 
Anilin-gentian-violet solution, formula 

for, 98 
Anthrax, 555 

bacilli, 556 
Anus, atresia of, 330 

Aorta, examination of arch of, before re- 
moval from body, 21 
aneurism of, 291 
atheroma of, 287 
malformations of, 269 



594 



INDEX. 



Aorta, stenosis of, 292 

Apoplectic clots, methods of examining, 12 

Apoplexy of brain, 185 

Arachnoid, nature of, 168 

Archiblast, 121 

Arnold, J., researches of, on lymphatic 

tissue in organs, 301 
Arsenic poisoning, lesions of, 584 
Arteries, aneurism of, 291 
atheroma of, 287 
cysts, atheromatous, of, 288 
dilatation of, 290 
effect of contraction of, in ob- 
literating endarteritis, 275 
inflammation of (see arteritis), 

285 
obliteration of, 292 
rupture of, 293 
stenosis of, 292 
tumors of, 294 
wounds of, 293 
Arteritis, acute, 285 
chronic, 285 
syphilitic, 286 
tubercular, 289 
Artery, hepatic, lesions of, 353 

mesenteric, emboli of, 334 
Arthritis, acute, 504 
chronic, 505 
deformans, 505 
gouty, 506 
purulent, 504 
rheumatic, 505 
sero-nbrinous, 504 
serous, 501 
tubercular, 506 
uritica, 506 
Arthropods, 81 
Ascaris lumbricoides, 76 
maritima, 77 
mystax, 77 
Ascites, tubercular, 346 
Aspergillus, 83 
Asphyxia, 575 
Ataxia, locomotor, 206 
Atelectasis, 235 
Atheroma, 287 
Atheromatous cysts, 288 

ulcers, 288 
Atrophia musculorum lipomatosa, 514 

Bacilli, chain-forms of, 88 
color-forming, 89 
curved-forms of, 88 
mobility of, 88 
pathogenic. 89 
Bacillus, 88 

anthracis, 556 

cholerse asiaticae, 538 

leprae, 558 

mallei, 560 

megaterium, 89 

of malignant oedema, 89 

of septicaemia of mice, 89 

tuberculosis, 252, 545 



Bacillus typhosus, 527 

Bacteria, 84 

action of disinfectants on, 86 
agar as culture medium for, 

101 
artificial cultivation of, 99 
as a cause of tumors, 120 
bibliography of, 103 
Brownian movement in, 87 
capsule of, 85 
classification of, 86 
cultivation of, 101 
facultative parasites, 91 
facultative saprophytes, 91 
filiform, 88 

gelatin nutrient as culture me- 
dium for, 100 
Gram's method for staining, 98 
in gangrene of the lung, 236 
influence of disinfectants on, 86 
influence of temperature on, 85 
involution forms in, 86 
methods of studying, 96 
mode of collecting specimens to 

be examined for, 103 
morphology and physiology of, 

84 
parasitic, 91 
plate cultures of, 101 
potatoes as culture medium for, 

100 
putrefaction dependent upon, 84 
relations of, to disease, 91 
rod-shaped, 88 
saprophytic, 91 
solid media for cultivation of, 

99 
spheroidal, 87 
spiral-shaped, 90 
spores of, 85 
staining agents for, 96 
zoogloea colonies of, 85 

Bacterial diseases, hereditary predisposi- 
tion to, 95 
diseases, conditior.s influencing 

occurrence of, 94 
origin of disease, proofs of, 94 

Balanitis, 472 

Beef-tea as culture medium for bacteria, 
101 

Belladonna poisoning, lesions of, 590 

Bile duct, examination of, at autopsies, 30 

Biliary passages, lesions of, 373 
passages, calculi of, 375 
passages, tumors of, 377 

Bilirubin in blood, 61 

Bismarck brown as bacterial stain, 96 

Bladder, gall, lesions of, 374 

urinary, calcification of, 285 
urinary, calculi in, 425 
urinary, in children, 42 
urinary, cysts of, 425 
urinary, dilatation of, 421 
urinary, diverticula of, 421 
urinary, foreign bodies in, 425 



INDEX. 



595 



Bladder, urinary, haemorrhage of, 422 
urinary, hernia? of, 422 
urinary, hyperemia of, 422 
urinary, hypertrophy of, 421 
urinary, inflammation of, 423 
urinary, malformations of, 420 
urinary, parasites of, 425 
urinary, perforation of, 422 
urinary, removal of, 32, 33 
urinary, rupture of, 422 
urinary, tumors of, 424 
Blood, air in, 61 

changes in circulation of, 53 
changes in composition of, 59 
coagulability of, 59 
diseases caused by alterations in 

composition of, 565 
distribution of, in life and death, 8 
extra vasated, changes in, 54, 55 
foreign bodies in, 61 
in Addison's disease, 565 
in Hodgkin's disease, 567 
in leukaemia and leucocythaemia, 60 
parasites in, 62 
Blood-vessels, atrophy of, 284 

degeneration, amyloid, 285 
degeneration, fatty, 284 
degeneration, hyaline, 285 
hypertrophy, 284 
inflammation of, 285, 296 
Bone, abscess, 489 

aneurism, 502 
atrophy, 499 
caries, 494 
cysts of, 503 
decalcifying, 43 
dislocations of, 483 
enostoses, 500 
exostoses, 500 
fractures of, 483 
haemorrhage, 483 
hyperaemia, 483 
hyperostosis, 500 
inflammation of (see osteitis) 484 
leukaemic, 498 
necrosis, 493 

necrosis by phosphorus, 494 
osteomalacia, 497 
osteomyelitis, 492 
parasites of, 503 
rachitic changes in, 495 
syphilitic congenital, 491 
tubercular, 490 
tumors of, 500 
wounds of, 483 
Bothriocephalus cordatus, 76 
cristatus, 76 
latus, 76 
Brain, abscess, 187 
anaemia, 184 

aneurism, miliary, of, 185 
apoplectic foci in, 185 
atrophy of, 193 

axis, mode of separation of, 13, 14 
cysts of, 190 



Brain, degeneration of, 182 

degeneration, secondary, of, 187 

dissection of, 11-14 

embolism, 181 

examination of, at autopsies, 11 

haemorrhage, 184 

haemorrhage, capillary, 185 

hernia, 195 

holes in, 190 

hyperaemia of, 184 

hypertrophy of, 193 

in new-born children, 40 

inflammation (see encephalitis), 

187 
inflammation, syphilitic, 190 
inflammation, tubercular, 191 
lesions of, in general paresis of in- 
sane, 192 
lobes, fissures, etc., 11 
membranes, lesions of, 163 
malformations of, 195 
mantle, mode of separation of, 

13, 14 
oedema, 184 
parasites, 195 
pigmentation, 194 
preservation and hardening of, 15 
sand, 166, 180 
sclerosis of, 189 
softening, red, of, 182, 187 
softening, white, of, 182 
softening, yellow, of, 182, 187 
thrombosis, 181 
tubercles, solitary, of, 192 
tumors of, 194 
ventricles of, 177 
weight of, 11 
wounds of, 189 
Bright's disease, acute, 403 

chronic, 409 
Bronchi, inflammation of (see bronchitis). 
227 
opening of, 23 
ossification, 230 
preservation of, 24 
tumors, 230 
Bronchiectasia, 229 
Bronchitis, capillary, 241 

catarrhal, acute, 227 
catarrhal, chronic, 228 
croupous, acute, 228 
croupous, chronic, 228 
Broncho-pneumonia, 241, 245 
Brood capsules of echinococcus, 74 
Brownian movement in bacteria, 87 
Burning, death from, 573 

Cacao butter for imbedding, 46 
Cachexia, development of, with malig- 
nant tumors, 118 
Cadaveric discolorations, 4 
Caecum, inflammation of, 336 
Calcareous degeneration, 68 
Calcification, 68 
Calculi, biliary, 375 



596 



INDEX. 



Calculi, pancreatic, 392 
prostatic, 481 
renal, 418 
vesical, 425 
Calvarium, examination of, at autopsies, 

9 
Cancer (see carcinoma), 150 
Cantharides poisoning, lesions of, 587 
Capillaries, blood, lesions of, 298 
Capsule in bacteria, 85 

suprarenal, examination of, at 

autopsies, 27, 42 
suprarenal, lesions of, 400 
Caput succedaneum, 38 
Carbonic acid poisoning, 591 

oxide poisoning, 590 
Carbolic acid poisoning, lesions of, 588 

acid, preservative action of, 49 
Carbuncle, 555 
Carcinoma, 150 

alveolar, 159 
cells, characters of, 151 
colloid, 159 

cylindrical-celled, 154-156 
n'bro-, 157 
fiat-celled, 153, 154 
forms of, 153 
gland-celled, 157 
medullary, 157 
melanodes, 160 
modes of extension, 152 
molle, 157 
myxomatodes, 159 
simplex, 157 
telangiectoides, 159 
Caries of bone, 494 
Carnoy's solution for fresh tissues, 43 
Casts, preservation of, 45 
Celloidin for imbedding, 46, 47 
Cephalhematoma, 39 
Cephalocele, 195 
Cercomonas intestinalis, 71 
Cestoda, 72 
Charcot's crystals, 567 
Cheeks, gangrene of, 312 

hypertrophy of, 311 
Cheesy degeneration, 64 

degeneration, tuberculous, 544 
Charbon, 555 

Children, new-born, autopsies on, 35, 
38 
new-born, changes in, immedi- 
ately following birth, 38, 39 
new-born, internal examina- 
tion of, 39-42 
Chloral hydrate poisoning, lesions of, 590 
hydrate, preserving action on 
tissues, 48 
Chloroform poisoning, lesions of, 589 

preserving action on tissues, 
48 
Chloroma, 135 
Chlorosis, 565 

Cholera asiatica, bacteria of, 538 
asiatica, lesions of, 537 



Cholera morbus, 332 

Cholestearin crystals in brain softening, 
182 
crystals in fatty degenera- 
tion, 65 
Cholesteatoma, 136 
Chondroma, 137 
Choroid plexus, cysts of, 180 

plexus, tumors of, 180 
Chromic acid for decalcifying, 44 

acid mixture for hardening tis- 
sues, 45 
Cicatricial tissue, 109 
Cirrhosis of the liver, 362 
Cirsoid aneurism, 290 
Clarke, columns of, in posterior spinal 

sclerosis, 207 
Clitoris, malformations of, 431 
Cloacae in intestine, 330 
Clots, apoplectic, in brain, 12, 185 

heart, 21, 22 
Cloudy swelling, 64 
Coagulation necrosis, 63 
Coccidium oviforme, 70 
CoJmheim's theory of embryonal origin of 

tumors, 119 
Colchicum poisoning, lesions of, 587 
Colitis, catarrhal, acute, 334 

catarrhal, chronic, 335 
croupous, 335 
Colloid carcinoma, 159 

degeneration, 67 
Colocynth poisoning, lesions of, 587 
Comma bacillus, 538 
Compound granular corpuscle, 183 
Condylomata, syphilitic, of penis, 472 
syphilitic, of vulva, 433 
Conium poisoning, lesions of, 590 
Consumption, 256 

Contusions, ante-mortem and post-mor- 
tem, 7 
Cooling of the body, post-mortem, 5 
Copper poisoning, lesions of, 586 
Cord, spinal, 199 
Coronary arteries, effects of closure of, on 

heart, 289 
Corpora anrylacea, 67, 180, 481 
Corrosive sublimate poisoning, lesions of, 

586 
Craniotabes, 497 
Creases in neck mistaken for marks of 

hanging, 7 
Croton-oil poisoning, lesions of, 587 
Croupous inflammation, 107 
Cryptorchismus, 474 
Cutis anserina, 577 
Cyanide of potassium poisoning, lesions 

of, 588 
Cyclopia, 195 
Cylindroma, 134 
Cysticercus celluloses, 72 

taenia mediocanellata, 73 
Cystin calculi, 426 
Cystitis, catarrhal, acute, 423 
chronic, 423 



INDEX. 



597 



Cystitis, croupous, 424 
tubercular, 424 
gangrenous, 423 
Cystocele, 422 
Cysto-sarcoma, 135 
Cysts, atheromatous, of aorta, 288 

classification of, 122 

congenital, 123 

dermoid, 123, 262, 425, 460 

echinococcus, 73, 74 

exudation, 123 

of bone, 503 

of parovarium, 460 

of softening, 123 

preservation of, for museums, 48 

retention, 123 



Death, causes of, 3 

sudden, from haemorrhage into 
floor of fourth ventricle, 186 
Decalcification of bone, 43 
Decomposition, post-mortem, 5 
Degeneration, acute, 113 
amyloid, 66 
calcareous, 68 
cheesy, 64 
colloid, 67 
fatty, 65 
hyaline, 68 
mucoid, 67 

parenchymatous, 64, 1.13 
Degenerations, secondary, in the nervous 

•system, 187, 199 
Delafield's osmic-acid mixture, 27, 44 
Dermoid cysts, 123, 262, 425, 460 
Diabetes, 571 
Diapedesis, haemorrhage by, 54 

in inflammation, 104 
Diaphragm, position of, 19, 40 
Digitalis poisoning, lesions of, 590 
Diphtheria, bacteria in, 536 

lesions of, 535 
Diphtheritic inflammation, 107 
Diplococcus, 87 

intracellularis meningitidis. 

534 
pneumoniae of Fraenkel, 238 
Discoloration, post-mortem, of body, 5 
Disinfectants, action of, on bacteria, 86 
Distoma haematobium, 72 
hepaticum, 71 
■ lanceolatum, 72 
sinense, 72 
Dochmius duodenalis, 77 
Double staining with eosin and baematoxy- 

lin, 47, 48 
Drowning, lesions of, 577 
Duodenum, removal of, from body, 29 

ulcers of, 334 
Dura mater, examination, post-mortem, 
of, 10 
mater, haemorrhage of, 163 
mater, inflammation of, 164 
mater, lesions of, 163 



Dura mater, thrombosis of longitudinal 
sinuses of, 163 
mater, tumors of, 167 
mater spinalis, inflammation of, 

(see pachymeningitis), 197 
mater spinalis, parasites of, 198 
mater spinalis, tumors of, 197 
Dyscrasia of tumors, 118 
Dysentery, 336 

Ecchondroses, 139 

Ecchymoses of skin, post-mortem, 7 

nature of, 54 
Ecchymosis, ante-mortem and post-mor- 
tem, 4 
Echinococcus, 73 

cysts, preservation of, for 
museums, 48 

exogena, 75 

multilocularis, 75, 372 

scolecipariens, 75 
Ehrlich's method of staining tubercle 

bacillus, 546 
Elaterium poisoning, lesions of, 587 
Elephantiasis, dilatation of lymph vessels 
in, 300 

of vulva, 433 
Embedding in celloidin, 46 
Emboli, fat, 61 

infectious, effects of, 58 
Embolic infarctions, most frequent seat of, 

58 
Embolism, effects and occurrence of, 56, 57 
Embryonal origin of tumors, Cohnheim's 

hypothesis of, 119 
Emigration of white blood-cells, 104 
Emphysema of lungs, 233 
Empyema, 223 
Encephalitis, 187 

chronic interstitial, 189 

in new-born, 190 
Encephalocele, 196 
Encephaloid cancer, 157 
Endarteritis, acute, 285 

chronic, 285 

obliterans, 286 

syphilitic, 288 

tubercular, 289 
Endartery (see terminal artery), 57 
Endocarditis, acute, 278 

bacteritic, 279 

chronic, 280 

malignant, 279 

mycotic, 279 

tubercular, 280 

ulcerative, 279 
Endocardium, structure of, 277 

discolorations of, 22 
fatty degeneration of, 275 
Endometritis, acute catarrhal, 442 

chronic catarrhal, 443 

croupous, 444 

puerperal, 445 

syphilitic, 444 

tubercular, 444 



598 



INDEX. 



Endophlebitis, 296 

Endothelioma, general characters and 

situation of, 136 
Endothelium of peritoneum, etc., em- 
bryonal origin of, 150 
Enostoses, 500 
Enteritis, catarrhal, acute. 332 

catarrhal, chronic, 333 
croupous. 333 
suppurative, 333 
Eosin, use of, in staining tissues, 47 
Ependyma, cysts of, 180 

examination of, at autopsy, 12 
inflammations of (see epen- 

dymitis), 178 
method of preserving, 15 
parasites of, 180 
tubercles of, 175 
tumors of, 180 
Ependymitis, acute and chronic, 178 

tubercular, 175 
Epiblast, tumors developed from, 121 
Epididymitis, acute, 476 
Epiglottis, inflammation near, 217 
Epispadia, 471 
Epithelial pearls in epithelioma, 156 

tumors, 146 
Epitheliomata, 153, 154 
Epulis, 132 

Erysipelas, characters of, 550 
micrococci of, 550 
Ether poisoning, lesions of, 590 
Exostoses, 139, 500 
Extra-uterine pregnancy, 462 
Extravasation of blood in contusions, 7 
Exudations, inflammatory nature and ori- 
gin of, 55, 104 
Eye, method of removal of, 15 

Fallopian tubes, changes in size and po- 
sition of, 461 
tubes, cysts of, 462 
tubes, dilatation of, 461 
tubes, haemorrhage of, 461 
tubes, inflammation of (see sal- 
pingitis), 461 
tubes, malformations of, 460 
tubes, position, shape, and di- 
mensions of, 34 
tubes, tumors of, 462 
False membrane in croupous inflamma- 
tion, 107 
neuromata, 143 
Famine fever, 531 

Farcy, characters and bacilli of, 559 
Fat embolism, 61 

necrosis in pancreas, 390 
pericardial, atrophy of, 276 
Fatty degeneration, 65 

infiltration, 65 
Favus, 83 

Female generative organs, removal of, 32 
generative organs, lesions of, 32, 
431 
Fever, inflammatory (see pyaemia), 552 



Fever, malarial, lesions and micro-organ" 
isms of, 562 
relapsing, 531 
relapsing, spirillum of, 531 
splenic, lesions and bacteria of, 

555 
suppurative (see pyaemia), 552 
surgical (see pyaemia), 552 
traumatic (see pyaemia), 552 
typhoid, 521 
typhus, 530 
Fibrin, formation of, in inflammation, 

104 
Fibro-carcinoma (scirrhus), 157 
Fibro-chondroma, 125 
Fibro-lipoma, 125 
Fibro-myxoma, 127 
Fibro-osteoma, 126 
Fibro-sarcoma, 126 
Fibroma, 125 

intracanalicular, 126, 467 
Filaria medinensis, 80 

sanguinis hominis, 80 
Fistula, recto-vaginal, 435 
vesico-vaginal, 435 
Flukes, 71 

Foetal tissues, preservation of, 42 
Foetus, size and appearance at different 

ages, 35-38 
Fourth ventricle of brain, opening of, 12 
ventricle of brain, haemorrhage in 
the floor of, 186 
Fractures, ante-mortem and post-mortem, 

8 
Fraenkel, pneumococcus of, 238 
Freezing microtomes, 43 
Fresh tissues, method of studying, 43 
Fuchsin as stain for bacteria, 96 
Fungi, parasitic, 83 
Fungus haematodes, 132 

of actinomycosis, 83 
of favus, 83 
of pityriasis, 83 
of ringworm, 88 
of thrush, 83 
poisoning, lesions of, 588 

Gall bladder, calculi of, 375 

dilatation of, 375 
inflammation of, 373 
opening of, at autopsies, 30 
tumors of, 377 
Gall ducts, calculi of, 375 

constriction and occlusion of, 

374 
dilatation of, 375 
inflammation of, 373 
tumors of, 377 
Gamboge poisoning, lesions of, 587 
Gangrene of the lung, 235 
Gastritis, catarrhal, acute, 321 
catarrhal, chronic, 321 
croupous, 322 
phlegmonous, 322 
suppurative, 322 



INDEX. 



599 



Gastritis, toxic, 323 

Gelatin culture medium for bacteria, 100 
Generative organs, female, lesions of, 431 
organs, removal and preserva- 
tion of, 32, 34 
organs, male, lesions of, 470 
organs, male, removal and pre- 
servation of, 32 
organs, of young children, 42 
Gentian-violet stain for bacteria, 96 
Giant cells in bone, 501 

cells in tubercle tissue, 113 
Giant-celled sarcoma, 132 
Glanders, 559 

bacilli of, 560 
Glioma, 139, 194 
Giio-rnyxoma, 140 

sarcoma, 131, 140 
Glossitis, superficial, 313 

parenchymatous, 314 
syphilitic, 314 
tubercular, 314 
Glottis, oedema of, 217 
Gluge's corpuscles, 183 
Glycerin not to be used to preserve fresh 

tissues, 49 
Goitre, 396 

Goll, columns of, in degeneration, secon- 
dary, of the spinal cord, 201 
columns of, in posterior spinal scle- 
rosis, 207 
Gonococcus, 429 
Gonorrhoea, 429 
Gout, 570 

joint lesions in, 506 
Gowers, columns of, in ascending gray 

degeneration, 201 
Gram's method of staining bacteria, 98 
Granulation tissue, 109 
Granulomata, infectious, 124 
Gray degeneration, secondary, in spinal 

cord, 200, 201 
Guinea-worm, 80 
Gummata, 113 
Gummy tumors, 113 

Hsematocele, 441, 475 
Haematoma, 54 
Haematometra, 435 
Haematophilia, 569 
Haematoxylin, formula for, 47 
Haematozoon of malaria, 564 
Haemorrhage, 53 

by diapedesis, 54 
by rhexis, 53 
Hasmorrhagic diathesis, 569 

infarction, 54, 57 
Hanging. 576 

Hardening and preserving tissues, 44 
Head, method of examination of, 9, 39 
Heart, abnormal size of. 270 

abscess of, 281 

aneurism of, 282 

atrophy of, 272 

atrophy of pericardial fat of, 276 



Heart, calcification of, 275 

changes in position of, 270 

children's, new-born, 40 

clot, 21, 22 

degeneration of, 274 

degeneration of, amyloid, 275 

degeneration of, fatty, 274 

degeneration of, parenchymatous, 
274 

dilatation of, 274 

exposed area of, 20 

fatty infiltration of, 276 

hypertrophy of, 272 

inflammation of (see myocarditis) 
281 

inflammation of endocardial 
lining, 277 

inflammation of, syphilitic, 282 

inflammation of, tubercular, 280 

malformations of, 268 

myomalacia of, 276 

opening cavities of, 21 

parasites of, 284 

preservation of tissues of, 23 

removal of, 21 

rupture of, 271 

size and position of, 20 

thrombosis of, 283 

tumors of, 284 

valves, aneurisms of, 282 

valves, fenestration of, 282 

valves, haemorrhage in, 282 

valves, sufficiency of, modes of de- 
termining, 21 

valves, position of, 21 

valves, vegetations on, 278, 280 

vegetations, 278 

walls, thickness of, 22 

weight of, 22 

wounds of, 271 
Hepatic veins, 355 
Hellebore poisoning, lesions of, 587 
Hepatitis, acute, 360 

chronic interstitial, 362 
purulent, 360 
syphilitic, 365 
tubercular, 366 
peri-, 368 
Hepatization, gray, in pneumonia, 238 

red, in pneumonia, 237 
Hermaphroditism, 471 
Hernias of bladder, 422 
of vagina, 434 
Histioid tumors, 121 
Hodgkin's disease, 309, 567 
Horseshoe kidney, 402 
Howship's lacunas in bone, 487 
Hyaline degeneration, 68 
Hydatids (see echinococcus), 73 
Hydatid moles, 128 
Hydraemia, 59 
Hydrencephalocele, 196 
Hydrocele, 474 
Hydrocephalus, 195 

acute, 177 



600 



INDEX. 



Hydrocephalus, congenital, 179 

external, 178 

internal, 178 

method of preserving 
brain in, 39, 40 

primary, in adults, 180 

secondary, 180 
Hydrochloric acid poisoning, 582 
Hydrocyanic acid poisoning, 588 
Hydromeningocele, 196 
Hydrometra, 438 
Hydromyelia, 209 
Hydromyelocele, 209 
Hydronephrosis, 416 
Hydrophobia, 561 
Hydrorrhachis, 209 
Hydro-salpinx, 461 
Hydrostatic test for aeration of lungs, 

41 
Hydrothorax, 218 
Hymen, malformations of, 431 
Hyperemia, 53 
Hyperostosis, 500 
Hypospadia, 470 
Hypostasis, post-mortem, 4 

Ichorrhsemia, 552 

Identity, observations regarding, at autop- 
sies, 4 
Imbedding, 46 

Incarceration of intestine, 330 
Indigo-sulphate poisoning, 580 
Infarction, 58 

haemorrhagic, from emboli, 

157 
white, 57 
of lungs, 232 
Infants, post-mortem examination of, 35 
Infectious diseases, relations of bacteria 

to, 91 
Infiltration, fatty, 65 
Inflammation, 104 

catarrhal, 105 
croupous, 107 
diphtheritic, 107 
exudative, 104 
parenchymatous, 114 
productive, 110 
scrofulous, 306 
suppurative, 106 
syphilitic, 113 
tubercular, 111 
Inflammatory fever (see pyaemia), 552 
Infusoria, 70 
Injection, interstitial, 45 
Injuries, post-mortem, 7 
Insolation, 572 

Intestines, appearances in, at autopsies, 
18 
atresia of, 330 
cadaveric lividities in, 29 
children's, new-born, 42 
cloacae of, 330 
concretions in, 338 
diverticula of, 329, 335 



Intestines, incarceration of, 330 

intussusception of, 331 

large, solitary follicles of, 336 

large, inflammation of, 334 

large, lymph nodules of, 336 

lesions of lymph nodes or 
glands of, 333 

lesions to be looked for at 
autopsies, 29 

malformations of, 329 

parasites of, 338 

preservation of, 29 

removal of, 28, 29 

rupture of, 332 

small, inflammation of (see 
enteritis), 332 

small, ulcers of, 332 

transposition of, 332 

tumors of, 337 

wounds of, 332 
Intracanalicular fibroma, 468 
Intussusception of intestine, 331 
Iodine test for waxy degeneration, 26, 67 
Irritants, vegetable, poisoning by, 587 
Itch insect, 81 



Jalap poisoning, lesions of, 587 

Joints, inflammation of (see arthritis), 504 

loose bodies in, 507 

tumors of, 507 

Kidney, gross appearance of, in health 
and disease, 26 
Bright's disease of, forms, 403 
calculi of, 418 
changes in position of, 402 
children, new born, in, 41 
congestion, acute, of, 403 
congestion, chronic, of, 409 
cystic, 416 

degeneration, acute, of, 403 
degeneration, amyloid, of, 413 
degeneration, chronic, of, 410 
degeneration, fatty, of, 404 
degeneration, parenchymatous, 

404 
degeneration, waxy, of, 26, 413 
embolism of, 415 
hydronephrosis, 416 
infarctions of, 415 
inflammation of (see nephritis), 

403 
inflammation, acute diffuse, 408 
inflammation, exudative, 404 
inflammation, suppurative, 413 
malformations of, 402 
method of opening and preserva- 
tion of, 25, 26, 27 
parasites of, 4<J0 
thrombosis of, 415 
tumors of, 418 
weight of, 26 

Lardaceous degeneration, 66 



INDEX. 



601 



Laryngitis, catarrhal, acute, 214 

catarrhal, chronic, 215 
croupous, 215 
syphilitic, 215 
tubercular, 216 
Larvnx, inflammation of (see laryngitis), 
214 
malformations of, 214 
preservation of, 25 
removal of, method, 24 
tumors of, 217 
Lead poisoning, lesions of, 586 
Leiomyoma, 557 
Lepra, 557 

bacilli of, 558 
Leprosy. 557 
Leptothrix buccalis, 90 
Leucocythamiia, 60, 567 
Leucocytosis, 60 
Leukaemia, 60, 309, 498, 567 ' 
Leukaemia, pseudo-, 309, 567 
Lightning, death from, 574 
Lipsemia, 61 
Lipoma, 137 

Lipomatosis of heart, 276 
Lips, gangrene of, 312 

hypertrophy of, 311 
Liver, abscess of, 360 

abscess of, bacteria in, 361 

abscess, metastatic, 361 

abscess, pyaemic, 361 

anaemia of, 351 

artery, hepatic, lesions of, 353 

atrophy of , 355 

atrophy, acute yellow, of, 359 

bronze, 358 

changes in position, 19, 351 

children, new born, in, 42 

cirrhosis of, 362 

cloudy swelling in, 355 

congestion of, 351, 352 

degenerations of, 355 

degeneration, amyloid, 357 

degeneration, fatty, 357 

degeneration, parenchymatous, 355 

degeneration, waxy, 357 

displacements of, 350 

fatty infiltration of, 356 

gummata of, 365 

haemorrhage of, 353 

hyperaemia of, 351 

inflammation of (see hepatitis), 360 

lymphatic tissue of, hyperplasia 
of, 368 

lymphomata, miliary, of, 368 

malformations of, 350 

nutmeg, 352 

parasites of, 371 

pigmentation of, 358 

preservation of, 31 

removal of, 30 

rupture of, 353 

situation of, 18 

size and weight of, 30 

tumors of, 369 



Liver, veins of, 353, 355 

wounds of, 353 
Lividity, cadaveric, 4 
Lobelia poisoning, lesions of, 590 
Locomotor ataxia, 206 
Louse, 81 
Lungs, atelectasis of, 235 

bacillus tuberculosis in, 263 
children stillborn, appearance of. 

41 
congestion of, 232 
emphysema of, 233 
examination, method of, 23, 24 
gangrene of, 235 
haemorrhage, 232, 233 
hydrostatic test for aeration of, 41 
infarctions of, 232 
inflammation of (see pneumonia), 

forms, 236 
inflammation of, syphilitic, 260 
inflammation of, tubercular, 250 
injuries of, 232 
malformations of, 231 
oedema of, 232 
parasites of, 263 
perforations of, 232 
preservation of, 24 
removal of, 23 
rupture of, 233 
tumors of, 262 
Lupus, 432, 548 
Lymph glands (see lymph nodes), 300 

glands, intestinal, lesions of, 333 

nodes, 300 

nodes, atrophy of, 308 

nodes, degenerations of, 307 

nodes, degeneration of, amyloid, 

308 
nodes, degeneration of, hyaline, 

308 
nodes, inflammation, acute, of, 301 
nodes, inflammation, chronic, of, 

303 
nodes, inflammation, syphilitic, 

307 
nodes, inflammation, tubercular, 

306 
nodes, inflammation, with cheesy 

degeneration of, 305 
intestinal lesions of, 333 
parasites of, 309 
pigmentation of, 304 
tumors of, 309 
nodules, 301 

nodules of large intestine, 336 
vessels, 299 

vessels, inflammation of, 299 
vessels, inflammation, syphilitic, 

of, 300 
vessels, inflammation, tubercular, 

of, 299 
vessels, tumors of, 300 
Lymphangitis, 299 
Lymphangiectasis, 300 
Lymphangioma, 145, 300 . 



602 



INDEX. 



Lymphatic tissue, 300 
Lymphomata, 124, 309, 368 
Lympho-sarcoma, 130 

Macroglossia, 300, 313 
Malarial fevers, lesions of, 562 

fevers, micro-organism, 562 
Malignant oedema, of mice, etc., 89 

pustule, 555 
Mamma, female, cysts, 467 

female, haemorrhage of, 165 
female, inflammation of (see 

mastitis), 465 
female, malformations of, 464 
female, tumors of, 467 
female, ulcers of, 467 
male, lesions of, 482 
Mastitis, acute, 465 

chronic, 466 
"Measly" pork, 72 

Mediastinum, general character of, 263 
inflammations of, 263 
tumors of, 264 
Melanaemia, 60 
Melano-carcinoma, 160 

sarcoma, 131 
Membranes, method of hardening, 45 
Meningitis, acute, 170, 171 

acute cerebrospinal, 533, 534 
chronic, 173 
exudative, 171 
syphilitic, 177 
tubercular, 173 
Meningocele, 196 
Mesoblast, 121 
Metaplasia, 138 
Metastasis in tumors, 117 
Methyl blue, stain for bacteria, 96 

violet, stain for amyloid, 66 
Metritis, acute, 444 

chronic, 444 
Microcephalia, 196 
Micrococci, color-forming, 87 

pathogenic, 87 
Micrococcus luteus, 87 
urese, 87 
Microcytes, 60 
Microtomes, 47 

freezing, 43 
Microscope for studying bacteria, 98 
Microsporon furfur, 83 
Miliary tubercles, 113 
Milk as culture medium for bacteria, 101 
Morbus maculosus, 568 
Moulds, 83 

Mouth, inflammation of (see stomatitis), 
311 
gangrene of, 312 
malformations of, 310 
tumors of, 312 
Mucin in mucoid degeneration, 67 
Mucoid degeneration, 67 
Mucous patches, 113 
Mutter's fluid, formula and uses, 44 
Mumps, 394 



Muscle, atrophy, simple, 512 

atrophy, progressive, 512 
degenerationof fatty, 515 
degeneration of hyaline, 515 
degeneration of waxy, 516 
haemorrhage of, 509 
hypertrophy of, 516 
infarction of, 509 
inflammation of (see myositis), 

509 
parasites in, 517 
pseudo-hypertrophy of, 514 
rupture of, 509 
tumors of, 516 
wounds of, 509 
Museum specimens, methods of preserva- 
tion, 48 
Mycosis intestinalis, 338, 556 
Myelitis, acute, 202, 203 

anterior cornua, of, 203 
chronic interstitial, 205 
chronic transverse, 205 
Myeloid sarcoma, 132 
Myeloplaxes, 501 
Myocarditis, 281 

interstitial, 281 
interstitial, chronic, 282 
purulent, 281 
syphilitic, 282 
Myoma, 141 

laevicellulare, 141 
striocellulare, 142 
Myomalacia of heart, 276 
Myositis, interstitial, chronic, 510 
ossificans, 511 
parenchymatous, 510 
suppurative, 509 
Myxoedema, 397 
Myxoma, 126 

gelatinosum, 127 
medullare, 127 
molle, 127 



Nabothi, ovula of, 443 

Nsevi, vascular, 145 

Necrosis, 63 

coagulation, 63 
of bone, 493 

Nematoda, 76 

Nephritis, 403 

chronic diffuse, with exuda- 
tion, 410 
chronic diffuse, without exu- 
dation, 411 
chronic pyelo-, 414 
diffuse, acute, 408 
diffuse, chronic, 410. 411 
exudative, acute, 404 
parenchymatous, acute, 403 
parenchymatous, chronic. 410 
peri-, 417 
suppurative, 413 
tubercular, 415 

Nerves, hardening of , 17 



INDEX. 



603 



Nerves, Weigerts method of staining 
with hematoxylin, 212 
peripheral, changes in, after divi- 
sion, 210 
peripheral, inflammation of (see 

neuritis), 210 
peripheral, tumors of, 212 
Nerve tissue, preparation of, 212 
Nervous system, lesions of, 163 
Neuritis, exudative, acute, 210 

interstitial, chronic, 211 
leprous, 212 
multiple, 211 
syphilitic, 211 
tubercular, 211 
Neuroglia, relations of, to connective tis- 
sue, 121 
Neuroma, 142 
Nitric acid poisoning, lesions of, 581 

acid, decalcifying for, 44 
Nitro-benzole poisoning, lesions of, 588 
Noma, 312, 432 
Nutmeg liver, 352 
Nux vomica poisoning, lesions of, 590 

Obliterating endarteritis, 286 
(Edema, 55 

glottidis, 217 
glottidis, post-mortem, 25 
malignant, of mice, 89 
Oesophagitis, catarrhal, 315 
croupous, 315 
<Esophagus, cysts of, 317 
dilatation, 316 
foreign bodies in, 316 
inflammation of (see oesopha- 
gitis), 315 
malformations of, 315 
preservation of, 25 
removal of, 24 
rupture of, 316 
stenosis of, 317 
tumors of, 317 
ulceration of, 316 
Oidium albicans, 83 
Omentum, 18 
Oophoritis, acute, 454 
chronic, 455 
syphilitic, 456 
tubercular, 456 
Opium poisoning, lesions of, 587 
Orchitis, acute, 476 
chronic, 476 
syphilitic, 479 
tubercular, 477 
Osmic acid as hardening agent, 45 
Osteitis, 486 

condensing, 488 
rarefying, 487 
suppurative, 489 
syphilitic, 490 
tubercular, 490 
Osteoblasts, 485 
Osteoclasts, 487 
Osteoma, 139 



Osteomalacia, 497 
Osteomyelitis, idiopathic, 492 
traumatic, 493 
Osteophytes, 139, 485 
Osteoporosis, 486 
Osteo-sarcoma. 133 
sclerosis, 486 
Ovarian cyst adenoma, 456 
Ovaries, cysts of, 454, 459, 460 

haemorrhage. 453 

hyperemia, 453 

inflammation of, 454 

malformations of, 453 

position, changes in, 453 

size, changes in, 453 

size and weight of, 34 

tumors of, 456 
Ovula NabotJii, 443 
Oxyuris vermicularis, 77 

Pacchionian bodies, 168 
Pachymeningitis, acute, 164 

chronic, 164 
hemorrhagic, 165 
syphilitic, 166 
tubercular, 166 
Pancreas, 390 

calculi in, 392 
degeneration of, 390 
displacements of, 393 
gangrene of, 391 
hemorrhage of. 389 
inflammation of (see pancreati- 
tis), 389 
malformations of, 329 
preservation of, 31 
removal of, 31 
size of, 31 
tumors of, 391 
Pancreatic ducts, dilatation of, 392 

foreign bodies in, 392 
Pancreatitis, interstitial, 390 

parenchymatous, 389 
suppurative, 390 
syphilitic, 390 
tubercular, 390 
Parablastic tissues, 120, 121 
Paraffin, 46 
Parametritis, 444 
Paraphimosis, 472 
Parasites, animal, 70 

methods of studying, 
82 
bibliography of, 82 
vegetable, 83 
Parasitic bacteria, 91 

fungi, 83 
Parenchymatous degeneration, 64 
Parotid gland, inflammation of, 394 
parasites of, 395 
tumors of, 305 
Parovarium, cysts of, 460 
Pearls, epithelial, 156 
Pediculus capitis, 81 
Penis, calcification of, 473 



604 



INDEX. 



Penis, enlargement of, 472 
haemorrhage of; 477 
inflammation of, 472 
injury of, 472 
malformations of, 470 
ossification of, 478 
tumors of, 472 
ulcers, phagedenic, of, 472 
ulcers, syphilitic, of, 472 
Periarteritis, 285 
Pericarditis, exudative, 267 
tubercular, 268 
Pericardium, 266 

dropsy of, 266 
haemorrhage of, 266 
inflammation of (see peri- 
carditis), 267 
injuries of, 266 
opening of, 20 
pneumonatosis of, 266 
tumors of, 268 
Perihepatitis, 368 
Perimetritis, 444 
Periostitis, acute simple, 484 
fibrous, 485 
ossifying, 485 
suppurative, 184 
syphilitic, 485 
tubercular, 486 
Periosteum, 484 
Periphlebitis, 296 
Perisplenitis, 385 
Peritoneum, 339 

inflammation of, 339 
malformations of, 339 
parasites of, 349 
tumors of, 347 
Peritonitis, acute, 340 

cellular, acute, 340 
cellular, chronic, 343 
chronic, with adhesions. 344 
chronic, with serum, fibrin, 

and pus, 345 
exudative, 340 
haernorrhagic, 346 
tubercular, 346 
Pernicious anaemia, 565 
Petechias, 54 
Phagocytes, 95 
Pharyngitis, catarrhal, 315 
croupous, 315 
submucous, 315 
Pharynx, inflammation of (see pharyngi- 
tis), 315 
lupus of, 316 
malformations of, 315 
preservation and removal of, 

24,25 
tumors of, 317 
ulceration of, 316 
Phimosis, 472 
Phlebectasia, 295 
Phlebitis, 296 

acute, 297 
syphilitic, 298 



Phlebitis, tubercular, 298 

uterine, 446 
Phleboliths, 56, 296 
Phosphorus poisoning, lesions of, 583 
Phthisis, acute catarrhal, 256 
acute pulmonary, 256 
chronic, 257, 258 
Pia mater, anaemia of, 169 

mater, blood-content of, 168 
mater, fatty degeneration in, 172 
mater, haemorrhage of. 169 
mater, hyperaemia of, 169 
mater, inflammation of, 170 
mater, oedema of, 169 
mater, parasites in, 177 
mater, pigmentation of, 177 
mater, removal of, 10 
mater, structure of, 167 
mater, tumors of, 177 
mater spinalis, 198 
mater spinalis, haemorrhage of, 198 
mater spinalis, inflammation of, 198 
mater spinalis, parasites of, 199 
mater spinalis, tumors of, 199 
Picric acid in decalcifying, 43 
Pigment in blood, 60 
Pigmentation, 69 
Pin worm, 77 
Pineal gland, 181 
Pituitary body, 181 
Pityriasis versicolor, 83 
Placenta, apoplexy of, 464 

degeneration of, 464 
haemorrhage in, 463 
inflammation of, 464 
Placentitis, chronic, 464 

suppurative, 464 
Plasmodium malariae, 563 
Plate cultures of bacteria, 101 
Pleura, 218 

haemorrhage of, 218 
hydrothorax, 218 
inflammation of, 218 
tumors of, 226 
Pleural cavities, air in, mode of detec- 
tion, 19 
examination of, 23 
Pleurisy, acute, 219 

artificial, in dog, 220 
chronic, 224 
subacute, 219 
tubercular, 224 
with effusion, 219 
with fibrin, 219 

with fibrin, serum, and pus, 223 
dry, 219 
Pleuritis (see pleurisy), 218 
Pneumococcus of Fraenkel, 238 

of Friedldnder, 236 
Pneumonia, acute lobar, 236 

acute lobar, with new con- 
nective tissue, 239 
broncho-, 241 
catarrhal, 241 
complicating, 246 



INDEX. 



605 



Pneumonia, forms of, 236 

interstitial, 248, 259 , 

of syphilis, 261 

lobar, 236 

lobular, 241, 246 

of heart disease, 24 T 

peribronchitic, 243 

secondary, 245 

syphilitic, 260 

tubercular, 249 
Pneumothorax, pyo-, 223 
Poisoning, lesions of, by aconite, 590 
lesions of, by alcohol, 588 
lesions of, by aloes, 587 
lesions of, by ammonia, 583 
lesions of, by arsenic, 584 
lesions of, by belladonna, 590 
lesions of, by cantharides, 587 
lesions of, by carbolic acid. 

588 
lesions of, by carbonic acid, 

591 
lesions of, by carbonic oxide, 

590 
lesions of, by chloral hydrate, 

590 
lesions of, by chloroform, 589 
lesions of, by colchicum, 587 
lesions of, by colocynth, 587 
lesions of, by conium, 590 
lesions of, by copper, 586 
lesions of, by corrosive subli- 
mate, 586 
lesions of, by croton oil, 587 
lesions of, by cyanide of potas- 
sium, 588 
lesions of, by digitalis, 590 
lesions of, by elaterium, 587 
lesions of, by ether, 590 
lesions of, by fungi, 588 
lesions of, by gamboge, 587 
lesions of, by hellebore, 587 
lesions of, by hydrochloric 

acid, 582 
lesions of, by hydrocyanic 

acid, 588 
lesions of, by jalap, 587 
lesions of, by lead, 586 
lesions of, by lobelia, 590 
lesions of, by nitric acid, 581 
lesions of, by nitrobenzole, 588 
lesions of, by nux vomica, 590 
lesions of, by opium, 587 
lesions of, by oxalic acid, 582 
lesions of, by phosphorus, 583 
lesions of, by potash, 582 
lesions of, by potassium ni- 
trate, 583 
lesions of, by potassium 

cyanide, 588 
lesions of, by savin, 587 
lesions of, by scammony, 587 
lesions of, by soda, 582" 
lesions of, by stramonium, 590 
lesions of, by strychnine, 590 



Poisoning, lesions of, by sulphuric acid, 
580 
lesions of, by tartar emetic, 

587 
lesions of, by tartaric acid, 582 
lesions of, by turpentine, 587 
lesions of, by veratria, 587 
lesions of, by vegetable irri- 
tants, 587 
removal of intestines and 
stomach in cases of, 28, 30, 
35 
Poliomyelitis anterior, 203 
Portal vein, dilatation of, 355 

vein, inflammation of, 354 
vein, lesions of, 353 
vein, rupture of, 354 
vein, thrombosis of, 354 
Post-mortem changes in abdominal 
organs, 18 
cooling of the body, 5 
decomposition, 5 
discoloration, 5 
examination in suspected 

poisoning, 35 
examination, external in- 
spection in, 4, 8 
examination, internal ex- 
amination in, 8 
examination, identity, ob- 
servations on, in, 4 
examination, reasons for 

making, 3 
fractures, 8 
hypostases, 4 
injuries, 7 

putrefactive changes, 4, 5 
rigidity or rigor mortis, 6 
temperature, elevation of, 

5, 6 
wounds, 8 
Potash poisoning, lesions of, 582 
Potassium cyanide poisoning, lesions of, 
588 
nitrate poisoning, lesions of, 
583 
Potato as culture medium for bacteria, 100 
Pregnancy, extra-uterine, 462 
Preservation of specimens, methods, 43 
Preserving fluid, temporary, for gross 

specimens, 48 
" Prickle " cells, 155 
Proglottides of tape worm, 72 
Prostate, atrophy of, 481 
calculi in, 481 
hypertrophy of, 480 
inflammation of, 481 
parasites in, 481 
tumors of, 481 
Protozoa, 70 

methods of study, 82 
Psammoma, 135 

of dura mater, 167 
Pseudo-hermaphroditism, 471 
leukaemia, 567 



606 



INDEX. 



Psorospermiae, 70 

Ptomaines, 92 

Pulmonary artery, thrombosis of, 233 

Purpura hemorrhagica, 568 

Purulent infection, 552 

Pus cells, 104 

Putrefactive bacteria, 84 

changes in body after death, 
4.5 
Pyaemia, bacteria in, 554 

nature and forms of, 552 
Pyelo-nephritis, 413 
Pyo- salpinx, 462 
Pyramidal tract, degeneration of, 200 

Rachitis, 495 

Ray fungus, 83 

Rectum, inflammation of, 336 

Relapsing fever, 531 

Respiratory system, 214 

Rhabdomyoma, 142 

Rhabdonema strongyloides, 81 

Rickets, 495 

Rigor mortis, 6 

Ringworm fungus, 83 

Saccharomyces albicans, 83 
Safranin for staining fresh tissues, 43 
Salivary glands, 394, 395 
Salpingitis, catarrhal, 461 
suppurative, 461 
syphilitic, 462 
tubercular, 462 
Salt solution for fresh tissue, 43 
Saprophytic bacteria, 91 
Sarcina, 88 
Sarcoma, 128 

adeno-, 135, 136 

alveolar, 134 

angio-, 133 

chondro-, 135 

cysto-, 135 

fibro-, 129 

giant-celled, 132 

glio-, 131 

lipo-, 135 

lympho-, 130 

melano-, 131 

myeloid, 132 

myo-, 135 

myxo-, 134 

round-celled, 130 

spindle-celled, 129 
Sarcoptes hominis, 81 
Savin poisoning, lesions of, 587 
Scammony poisoning, lesions of, 587 
Scars, disappearance of, in skin, 8 
Scirrhus, 157 
Sclerosis, multiple, of cord, 205 

posterior spinal, 206 
Scolex of tape-worm, 72 
Scolices of echinococcus, 74 
Scorbutus, 568 
Scrofula, 306 



Scrotum, lesions of, 473 
Scurvy, 568 
Section cutting, 46, 47 
Seminal vesicles, 480 
Septicaemia, 552 

of mice, bacilli of, 89 
Septo-pyaemia, 552 
Serum in inflammation, 104 

post-mortem accumulation of, in 
pleural cavities, 23 
Skull, examination of, from within, 14, 15 

cap, 9 
Soda poisoning, lesions of, 582 
Solitary tubercles of brain, 192 
Spermatocele, 475 

Specimens, importance of good preserva- 
tion of, 49 
Spider cells, 140 
Spina bifida, 209 
Spinal cord, 199 

cord, children's, 40 

cord, degeneration, grav, of, 199,. 
200, 201 

cord, examination of, 16, 17 

cord, gummata of, 207 

cord, haemorrhage of, 199 

cord, inflammation of, 202 

cord, inflammation, syphilitic, of, 
207 

cord, inflammation, tubercular, of, 
207 

cord, injuries of, 199 

cord, malformations of, 209 

cord, membranes of, 197 

cord, posterior sclerosis in, 206 

cord, preservation of, 17 

cord, removal of, 16 

cord, sclerosis of, 200, 205 

cord, syringomyelia, 208 

cord, tumors of, 207 
Spiral-shaped bacteria, 90 
Spirillum cholerae asiaticse, 538 
fever, 531 
rugula, 90 
serpens, 90 
Spiro-bacteria, 90 
Spirochaete denticola, 90 

Obermeieri, 531 
plicatitis, 90 
Spleen, abscess, 382 

anaemia of, 379 

appearances of, 28 

atrophy of, 386 

children's, 42 

congestion, acute, 380 

degenerations of, 386, 390 

displacements of, 387 

haemorrhage of, 379 

hyperaemia of, 379 

infarctions of, 380 

hyperaemia of, 379 

inflammation of (see splenitis), 381 
leukaemic, 385 

malarial, 382 

malformations of, 387 



INDEX. 



607 



Spleen, nature of, 378 
parasites of, 387 
pigmentation of, 386 
preservation of, 28 
rupture of, 378 
size, etc., of, 27, 28 
tumors of, 387 
wounds of, 378 
Splenic fever, 555 

tumor, chronic, 382 
Splenitis, acute hyperplastic, 381 
chronic indurative, 382 
peri-, 385 
suppurative, 382 
syphilitic, 383 
tubercular, 383 
Spores of bacteria, 85 
Staining methods of, 47 
Staphylococcus pyogenes aureus in gan- 
'grene of the lungs, 236 
pyogenes aureus in malig- 
nant endocarditis, 279 
pyogenes aureus in py- 
aemia, 554 
pyogenes aureus in sup- 
puration, 106 
Stomacace, 311 

Stomach, degenerations of, 329 
dilatation of, 326 
diphtheritic inflammation of, 322 
erosions, haemorrhagic, of, 326 
haemorrhage, 320 
inflammation of (see gastritis), 

321 
injuries of, 320 
malformations of, 319 
preservation of, 30 
post-mortem changes in, 320 
removal of, 29 
situation of, 19 
tumors of, 326 
ulcers of, 323, 326 
Stomatite, ulcero-membraneuse, 311 
Stomatitis, catarrhal, 311 
croupous, 311 
syphilitic, 312 
tubercular, 312 
ulcerosa, 311 
Stramonium poisoning, lesions of, 590 
Strangulation, 576 
Strawberry marks, 145 
Streptococci, 87 

in uterine phlebitis, 446 
Streptococcus diphtheriae, 536 

erysipelatos, 550, 551 
pyogenes in inflammation, 

106 
pyogenes in malignant en- 
docarditis, 279 
pyogenes in pyaemia, 554 
Strongylus gigas, 77 

longevaginatus, 77 
Struma, 396 

Strychnia poisoning, lesions of, 590 
Sublingual gland, 394, 395 



Submaxillary gland, 394, 395 

Suffocation, 575 

Suggillations, 54 

Sulphuric acid poisoning, lesions of, 580 

Sunstroke, 572 

Suppurative fever, 552 

Suprarenal capsules, children's, 42 

capsules, degeneration of, 400 
capsules, examination of, 27 
capsules, haemorrhage of, 400 
capsules, in Addison's disease, 

566 
capsules, inflammation of, 400 
capsules, malformations of, 400 
capsules, preservation of, 27 
capsules, size of, 27 
capsules, thrombosis in, 400 

Surgical fever, 552 

Syphilis, congenital, bones in, 491 

Syphilitic inflammation, 113 

Syringomyelia, 208 

Taenia cucumerina, 76 
echinococcus, 73 
flavo-punctata, 76 
madagascariensis, 76 
mediocanellata, 72 
nana, 75 
saginata, 72 
solium, 72 
Tape worm, 72 

Tartar emetic poisoning, lesions of, 587 
Tattoo marks, disappearance of, 8 
Temperature, post-mortem elevation of. 

5, 6 
Teratoma, 122 

myxomatodes, 264 
Terminal artery, 57 
Testicle, atrophy of, 474 
cysts of, 480 
gummata of, 479 
haematocele, hydrocele, sperma- 
tocele, 475 
inflammation of (see orchitis), 

476 
malformations of, 474 
parasites of, 480 
preservation of, 32 
removal of, 32 
size of, 32 
tumors of, 479 
Thorax, examination of organs of, 17, 20 
Thrombi, causes of, 55, 56 
changes in, 56 
forms of, 56 
Thrombosis, 55 

of portal vein, 354 
of venous sinuses of dura 
mater, 163 
Thrombus, 55 
Thrush, 83 
Thymus, 40, 399 
Thyroid gland, atrophy of, 397 

gland, degeneration of, 396 
gland, hyperaemia of, 396 



608 



INDEX. 



Thyroid gland, in myxcedema, 397 
gland, inflammation of, 396 
gland, parasites of, 397 
gland, preservation of, 25 
gland, removal of, from body, 

25 
gland, tumors of, 396 
gland, weight of, 25 
Tongue, hypertrophy of, 313 
inflammation of, 313 
malformations of, 313 
tumors of, 314 
Trachea, inflammation of. 214 
malformations of, 214 
tumors of, 217 
Transudation, 55 
Traumatic fever, 552 
Trematoda, 71 
Trichina spiralis, 78 
Trichomonas vaginalis, 71 
Trichophyton tonsurans, 83 
Tricocephalus dispar, 78 
Tubercle bacilli, characters of, 545 
bacilli, cultivation of, 547 
bacilli, in tuberculosis, 542 
bacilli, staining of, 546 
granula, 113, 544 
tissue, 543 
Tubercles, from which bacilli are absent, 
545 
miliary, 113, 543 
solitary, 192 
Tubercular inflammation, 111 
Tuberculosis, acute miliary, 250 

bacillus of, in lungs, 263 
bibliography of, 547 
chronic miliary, of lungs, 

254 
nature of, 542 
role of bacilli in, 542 
subacute miliary, 253 
Tumors, bacteria in, 120 
benign, 117 
bibliography, 160 
cause of, 119 
cells of, negative character of, 

120 
characters, general, of, 115 
classification of, 120 
complex congenital, 122 
complex nomenclature of, 124 
connective tissue, 121 
embryonal origin of, 119 
epithelial, 146 
fibro-cystic, 449 , 
growth, mode of, 116 
heterologous, 115 
histioid, 121 
homologous, 115 
malignant, 117 
metastasis of, 117 
mixed forms of, 122 
preservation of, 124 
shapes of, 116 
special forms of, 125 



Tumors, teratoid, 122 

Tiirck, columns of, in, gray degeneration 
of cord, 200 

Turpentine poisoning, lesions of, 587 

Typhoid bacillus, 527 

bacillus, staining, 528 

fever, bacillus of, 527 

fever, blood-vessels, lesions in, 526 

fever, brain lesions in, 526 

fever, croupous enteritis in, 524 

fever, gangrene of intestine in, 

523 
fever, haemorrhage in, 524 
fever, heart lesions in, 525 
fever, infarctions in, 524 
fever, kidney lesions in, 526 
fever, liver lesions in, 525 
fever, lung lesions in, 526 
fever, lymphatic structures of 

intestines, lesions of. in, 522 
fever, mesenteric glands in, 524 
fever, mouth in, 525 
fever, muscle lesions in, 527 
fever, parotid lesions in, 525 
fever, Peyer's patches in, 522 
fever, pharynx lesions in, 525 
fever, skin lesions in, 527 
fever, spleen lesions in, 524 

Typhus fever, 530 

recurrens, 531 

Ulcers, duodenal, in burns, 573 
Umbilical cord, changes in, after birth, 

38 
Ureter, examining of, 25 
Urethra, dilatation of, 427 

inflammation of (see urethritis), 

428 
malformations of, 427 
perforations of, 428 
prolapse of, 428 
rupture of, 428 
strictures of, 427 
tumors of, 430 
ulcers of, 430 
wounds of, 428 
Urethritis, catarrhal, 428 
croupous, 430 
gonorrheal, 429 
tubercular, 430 
Urinary apparatus, 402 
Uterine mucous membrane, hyperplasia 

of, 447 
Uterus, carcinoma of, 450 
cysts of, 452 

degeneration, amyloid, of, 447 
degeneration, fatty, of, 446 
diminution in size of, 437 
enlargement of, 437 
hematocele of, 441 
haematometra, 488 
haemorrhage of, 441 
herniae of, 440 
hydrometra, 438 
hyperaemia of, 440 



INDEX. 



609 



Uterus, infant's, 34 

inflammation of (see metritis and 

endometritis), 442, 445, 446 
malformation of, 436 
malpositions of, 438 
parasites of, 452 
perforation of, 440 
polypi in mucous membrane of, 

447 
rupture of, 440 
size of, S3 
tumors of, 447 
ulceration of, 446 

Vagina, cysts of, 436 

dilatation of, 434 

examination of, 33 

fistalse of, 435 

gangrene of, 436 

hernias of, 434 

inflammation of (see vaginitis), 

435 
lengthening of, 434 
malformations of, 433 
narrowing of, 434 
parasites of, 436 
perforations of, 435 
prolapse of, 434 
tumors of, 436 
wounds of, 435 
Vaginitis, catarrhal, 435 
croupous, 435 
suppurative, 435 
syphilitic, 436 
tubercular, 436 
Vascular system, 266 
Vein stones, 56 ' 
Veins, dilatation of, 295 

hepatic lesion of, 355 
inflammation of (see phlebitis), 296 
inflammation, syphilitic, of. 298 
inflammation, tubercular, of, 298 
parasites in, 298 
perforation of, 296 



Veins, phlebectasia, 295, 296 

phleboliths, 296 

rupture of, 296 

tumors of, 298 

wounds of, 296 
Veratria poisoning, lesions of, 587 
Vermiform appendix, 336 
Vernix caseosa, 38 
Vulva, cysts of, 433 

gangrene of, 432 

haemorrhage of, 431 

hyperemia of, 431 

inflammation of, 432 

lupus of. 432 

malformations of, 431 

noma of, 432 

oedema of, 432 

tumors of, 432 

Water tests for heart valves, 21 
Wax for imbedding, 46 
Waxy degeneration, 66 

degeneration, tests for, 26 
Weigerfs hematoxylin method for stain- 
ing nerve tissue. 212 
Whip worm, 78 
Worms, 71 
Worm, guinea, 80 

pin, 77 

round, 76 

tape, 72 

thread, 77 

whip, 78 
Wounds, post-mortem, 8 

Xanthin calculi, 426 

Yeasts, 83 
Yellow fever, 541 

ZieJiVs solution for staining bacteria, 528 
Zoosrloea colonies of bacteria, 85 



49 



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